case study on effects of industrial pollution

• Open access
• Published: 18 June 2021

Is industrial pollution detrimental to public health? Evidence from the world’s most industrialised countries

• Mohammad Mafizur Rahman 1 ,
• Khosrul Alam 2 &
• Eswaran Velayutham 1  

BMC Public Health volume  21 , Article number:  1175 ( 2021 ) Cite this article

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Industrial pollution is considered to be a detrimental factor for human health. This study, therefore, explores the link between health status and industrial pollution for the top 20 industrialised countries of the world.

Crude death rate is used to represent health status and CO 2 emissions from manufacturing industries and construction, and nitrous oxide emissions are considered to be indicators of industrial pollution. Using annual data of 60 years (1960–2019), an unbalanced panel data estimation method is followed where (Driscoll, J. C. et al. Rev Econ Stat, 80, 549–560, 1998) standard error technique is employed to deal with heteroscedasticity, autocorrelation and cross-sectional dependence problems.

The research findings indicate that industrial pollution arising from both variables has a detrimental impact on human health and significantly increases the death rate, while an increase in economic growth, number of physicians, urbanisation, sanitation facilities and schooling decreases the death rate.

Conclusions

Therefore, minimisation of industrial pollution should be the topmost policy agenda in these countries. All the findings are consistent theoretically, and have empirical implications as well. The policy implication of this study is that the mitigation of industrial pollution, considering other pertinent factors, should be addressed appropriately by enunciating effective policies to reduce the human death rate and improve health status in the studied panel countries.

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Introduction

The link between environmental pollution and human health is discussed in a variety of literature, and is still a crucial issue of research, especially in the current COVID-19 pandemic situation. Environmental pollution contributes to climate change, which has various negative impacts on human health like perinatal disorders, infant mortality, respiratory disorders, allergies, malignancies, cardiovascular disorders, increase in oxidative stress, endothelial dysfunction, and mental disorders [ 1 , 2 ]. The impacts on health can be so severe that they lead to death; nearly 7 million people die every year from the interaction of fine particles in polluted air (Goal- 3 of SDGs, [ 3 ]). Global environmental pollution is largely a result of people’s activities through urbanization, industrialization, large-scale petrochemical use, power generation, heavy industry, and mining and exploration, all of which adversely affect the health of local communities through their working and residential actions [ 4 , 5 ]. Therefore, the matter of pollution distress has attracted contemporary global attention due to its acute long-run consequences on human health. Despite this global attention, there are still some policy uncertainties in the existing strategies due to the lack of a wide-ranging and comprehensive study that clearly addresses the adverse impact of industrial pollution on human health status.

Against this backdrop, this study has considered the connection between industrial pollution and health status in the world’s 20 most industrialised countries (see section 3.1). These countries have a total population of 4.57 billion (60% of the world’s population) where the total real GDP is US$66347.02 billion, reflecting 78.18% of the world’s real GDP [ 6 ]. The industrial value addition of these countries is US$17,783.95, which is 75.38% of world’s total industrial value addition [ 6 ]. The average crude death rate in this region is 8.23 per 1000 population, while the total CO 2 emissions are 25,576.7 million tonnes covering 74.85% of the world’s emissions, and the nitrous oxide emissions are 18,37,026.82 thousand metric tons of CO 2 equivalent, which is 58.25% of the world’s emissions [ 6 , 7 ]. Hence our study is comprehensive and explores a vital issue in relation to both the environment and human health.

Some past studies (see [ 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 ], among others) have attempted to discover the factors that have impacts on human health and the death rate. However, based on their contradictory findings it has been difficult to draw conclusive and comprehensive guidelines for formulating certain policy initiatives. An inclusive and rigorous probe is necessary to achieve effective policy recommendations. From this perspective, this study is a conscientious venture to reduce the death rate by mitigating industrial pollution, considering the other controlled variables like economic growth, medical attention, drinking water services, sanitation services, secondary school enrolment and urbanisation in a panel of world’s most 20 industrialised countries.

The rationale for considering the desired variables lies in both the theoretical and conceptual notions and previous literary works. The CO 2 and nitrous oxide emissions create industrial pollution which leads to the increase in the human death rate by generating pollution borne diseases ([ 12 , 13 , 17 , 18 , 19 , 20 , 21 , 22 , 23 ]; and [ 24 ]). Similarly, having access to the required number of physicians also plays an important role in reducing the mortality rate by providing more effective health care services ([ 11 , 25 , 26 , 27 , 28 ]; and [ 29 ]). The access to clean water facilities, another vital element, decreases the death rate by satisfying basic needs (see [ 14 , 16 , 27 , 30 , 31 ]). Adequate and sufficient sanitation facilities also play a significant role in improving human health and reducing the mortality rate by maintaining safety and hygiene [ 8 , 14 , 15 , 16 , 27 , 30 , 31 , 32 ]. In the same way, education facilities help to increase awareness about health consciousness and this may play a role in lowering the death rate ([ 10 , 33 , 34 , 35 ]; Ray and Linden, 2020 [ 8 , 25 ];). While a greater urbanisation rate increases different health related amenities which reduces mortality rate on the one hand, it also increases mortality by increasing pollution due to different urban activities ([ 9 , 16 , 17 , 32 , 36 , 37 ]; and [ 27 ]). Therefore, more detailed investigation is still needed to assess the role of associated elements on human health.

The major contributions of this study can be noted as: (i) to the best of our knowledge, this is the first study in the literature that investigates the causative elements of the death rate in 20 of the world’s most industrialised countries; (ii) this study has used the most recent and wide-ranging data period of 60 years (1960-2019); (iii) the robust outcomes are achieved by employing an rigorous econometric approach like Driscoll and Kraay’s [ 38 ] standard error technique (details are in section 3.3); (iv) comprehensive policy recommendations, based on the results, are delivered for researchers and policy makers to address the issue of industrial pollution along with other relevant factors for reducing the death rate and improving human health by undertaking effective policy measures.

This research is designed in the following manner: following the introduction, section 2 provides the review of the past literatures; section 3 explains the data and methodology; section 4 displays and analyzes the empirical results; and section 5 provides the conclusion and policy recommendations.

Literature review

Industrial pollution has many adverse consequences on human health and may be a cause of death because of respiratory, lung and cardio-related diseases (see [ 12 , 13 , 17 , 18 , 19 , 20 , 21 , 22 , 23 ]; and [ 24 ], among others). Leogrande et al. [ 13 ] discovered the significant impact of industrial air pollution on respiratory mortality in the Taranto area, Southern Italy by applying a difference-in-differences approach from the data of 1998–2014. Further, Karimi and Shokrinezhad [ 12 ] observed that PM 2.5 , PM 10 , CO, NO 2 , and SO 2 were positively and significantly linked with both infant and child under-five mortality for 27 countries for the data period of 1992–2018. Bauleo et al. [ 19 ] found a positive association between industrial PM 10 and mortality from non-accidental causes, all cancers, and cardiac diseases, for the industrial area of Civitavecchia, Italy. Similarly, Næss et al. [ 21 ] identified that the air pollutant indicators (NO 2 , PM 10 , and PM 2.5 ) had a significant effect on all causes of death for both men and women in Oslo, Norway. Similar findings were also identified in the works of Anwar et al. [ 18 ] for 12 of the most vulnerable Asian countries, Shan et al. [ 23 ] for China, Lehtomäki et al. [ 20 ] for Nordic countries, Rajak and Chattopadhyay [ 22 ] for India, and Brito [ 39 ] for Portugal. Clancy et al. [ 40 ] maintained that control of the particulate air pollution significantly reduces the death rate from the comparison of pre and post 72 months ban on coal sales in Dublin, Ireland. In case of CO 2 related pollution, Duong and Jayanthakumaran [ 41 ] found that an increase in CO 2 emissions caused poor health for 60 provinces in Vietnam. Shobande [ 16 ] also demonstrated that the CO 2 emissions increased infant and child mortality in the case of 23 African countries. Dedoussi et al. [ 42 ] and Im et al. [ 43 ] obtained evidence of pre-mature mortality due to cross state air pollution in the USA, and in four Nordic countries, respectively. In the case of the COVID-19 pandemic, Fareed et al. [ 24 ] ascertained that air pollution led to the increase of COVID-19 related mortality in Wuhan, China where daily data from 21 January 2020–31 March 2020 were used. Similar findings of COVID-19 related mortality were also observed by Coker et al. [ 44 ] for northern Italy, Isphording and Pestel [ 45 ] for Germany, Marquès et al. [ 46 ] for Spain, and Gupta et al. [ 47 ] for nine Asian cities. On the other hand, Karuppasamy et al. [ 48 ] found that the improved air quality due to reduced pollution decreased the mortality rate due to COVID-19 for India. However, Cheung et al. [ 49 ] obtained the statistically insignificant impact of the air pollution on cardio-respiratory mortality in Hong Kong. In their studies, the researchers did not focus on the rigorous estimation regarding the impact of the CO 2 emissions and nitrous oxide emissions as outcomes of industrial pollution on the death rate, considering the panel of most industrialised countries.

Some works that considered CO 2 emissions on the relationship with other variables were also found; in the literature (see Mehmood [ 50 ] for Singapore, and Mehmood and Tariq [ 51 , 52 ], and Mehmood et al. [ 53 , 54 ] for South Asian countries; Mehmood et al. [ 50 ] for 3 developing countries, and Mehmood [ 54 ] for South Asian countries). However, these studies did not show the impact of CO 2 emissions, along with other relevant factors, on human health.

Thus, more critical analysis regarding the effect of industrial pollution on human health covering the most industrialised countries deserves further attention.

The death rate in a country is also related to the number of physicians employed in that country (see [ 11 , 25 , 26 , 27 , 28 ]; and [ 29 ], among others). In this context, Jebeli et al. [ 11 ] found that there is a strong reverse correlation between the number of physicians and the crude death rate in the case of 26 OECD countries for the period 2000–2012. Muldoon et al. [ 27 ] found that higher physician density rate worked as the significant reducing factor of infant and child mortality rate in the context of 136 UN member countries, where a mixed effects linear regression model based on 2008 cross-sectional data is employed. In the same way, Farahani et al. [ 25 ] found that the physician density reduces infant mortality both in the short run and long run, where global data of 1960–2000 are used. Using semi-parametric analysis, Liebert and Mäder [ 26 ] also observed that higher physician density reduced infant mortality in Germany from the data of 1928–1936. Russo et al. [ 28 ] found that the supply of primary care physicians contributed to the reduction of infant mortality in Brazil during 2005–2012. Shetty and Shetty [ 29 ] also concluded that the number of doctors per capita had an opposing affiliation with the mortality rate in the case of Asian countries. The role of more physicians in the most industrialised countries to ensure lower mortality rate has not been observed in the past literature. Therefore, inclusion of the number of physicians or its density in death rate analysis is essential to reaffirm its role.

Access to clean water facilities can also influence the mortality rate (see [ 14 , 16 , 27 , 30 , 31 ], among others). Ezeh et al. [ 31 ] found that the risk of mortality from unimproved water was significantly higher in Nigeria, where pooled data of 2003, 2008 and 2013 of Nigeria Demographic and Health Survey were used. Likewise, applying ordinal logistic regression, Cheng et al. [ 30 ] observed that the access to water significantly reduced infant, child, and maternal mortality in the case of 193 countries. Similar results were also found by Muldoon et al. [ 27 ] for 136 UN member countries. Lu et al. [ 14 ] ascertained that improved water facilities reduced the infant mortality rate in the case of 84 developing economies during 1995–2013. In contrast, Shobande [ 16 ] found no significant impact of improved water sources on infant and child mortality in 23 African countries. More research related to the necessity of access to clean water in the panel of industrial countries is urgently needed, but is not found in the existing literature. These findings have emphasised the need for more exploration of the importance of access to clean water facilities on the mortality rate.

The importance of sanitation facilities on the mortality rate cannot be ignored and a number of studies have revealed their role (see [ 8 , 14 , 15 , 16 , 27 , 30 , 31 , 32 ]; among others). Rahman et al. [ 15 ] found that sanitation facilities significantly reduced the crude death rate and infant mortality rate in the case of 15 SAARC-ASEAN countries for the data period of 1995–2014 where fixed effect, random effect and GMM estimator were employed. Ezeh et al. [ 31 ] also found the impact of unimproved sanitation facilities on mortality in Nigeria. Lu et al. [ 14 ] and Alemu [ 8 ] observed that improved sanitation facilities reduced infant mortality rate for 84 developing economies, and for 33 African countries, respectively. Likewise, Cavalcanti et al. [ 32 ] found that the household sanitary facilities reduced child mortality in Brazil. Furthermore, Shobande [ 16 ] discovered that sanitation facilities had a significant impact on infant and child mortality in 23 African countries. In the same way, Muldoon et al. [ 27 ] and Cheng et al. [ 30 ] found that access to sanitation facilities reduced infant, child, and maternal mortality for 136 UN member countries and for 193 countries, respectively. However, in the previous studies, the importance of sanitation facilities on death rate in terms of a panel of most industrialised countries has been ignored. Thus it is important to identify the nexus between sanitation facilities and the mortality rate as a way of implementing improved policy initiatives.

Education reduces the mortality rate by increasing consciousness and responsiveness, as explicated in a number of empirical works, for example Halpern-Manners et al. [ 10 ], Doniec et al. [ 34 ], Buckles et al. [ 33 ], Sajedinejad et al. [ 35 ], Ray and Linden (2020), Alemu [ 8 ], Farahani et al. [ 25 ], among others. Halpern-Manners et al. [ 10 ] observed the robust relationships between education and mortality in the case of the USA. Similarly, Doniec et al. [ 34 ] discerned that those in lower educational groups were significantly more likely to die in the case of 3 Eastern European countries covering the period of 1982–2013. Buckles et al. [ 33 ] also found that college education reduced the mortality in Vietnam. Furthermore, Sajedinejad et al. [ 35 ] identified that education reduced the maternal mortality rate in 179 countries Ray and Linden (2020) observed that the primary education rate significantly reduced infant mortality in 195 countries during the data period of 1995–2014. Similar statistics were also been obtained by Alemu [ 8 ] in the case of 33 African countries from 1994 to 2013. However, Farahani et al. [ 25 ] and Anwar et al. [ 18 ] found no statistically significant impact of education on infant and neonatal mortality for the global panel and the 12 most vulnerable Asian countries, respectively. By critically analysing the research, it has been observed that past studies did not consider the significance of education in determining the death rate in the panel of most industrialised countries. Therefore, because the nexus between education and mortality is not clear, there is a need for investigations into this issue.

Urbanization can also play a significant role in the mortality rate. In this perspective, Bandyopadhyay and Green [ 9 ] found evidence of robust negative correlation between crude death rate and urbanization in the case of the global context. However, Brueckner [ 36 ] found no significant negative correlation between adult mortality and urbanization in sub-Saharan Africa during the data period of 1960–2013. Similarly, Wang [ 37 ] found that the increase in urbanization is significantly linked with reduced mortality, under-five mortality, and infant mortality in 163 countries during 1990–2012, and the effect is stronger in high-income nations. In contrast, Cavalcanti et al. [ 32 ] observed that the urbanization rate significantly increases child mortality in Brazil. Similarly, Taghizadeh-Hesary et al. [ 17 ] found that the urbanization rate increased the risks of lung and respiratory diseases in the case of 18 Asian countries. However, Shobande [ 16 ], and Muldoon et al. [ 27 ] found no significant impact of urbanization on infant and child mortality for 23 African countries, and for 136 UN member countries, respectively. The consideration of urbanization in the context of the panel of highly industrial countries has not been found in previous literature. Moreover, the ambiguous identification of impact of urbanization on mortality rate demands more thorough investigation.

From the current literature it may be observed that the existing identifications regarding the impact of industrial pollution, density of physicians, access to clean water and sanitation facilities, education, and the urbanization rate on human health status are not unanimous and conclusive. Furthermore, the findings of the noted determining factors on the death rate as a group in the world’s most 20 industrialised countries are absent. Therefore, the present study is an endeavour to fill up the existing literature gap to formulate efficacious and durable policy in the health sector.

Data and methodologies

Selection of countries.

This study explores the relationship between health status and industrial pollution in the world’s 20 most industrialised countries. Based on manufacturing, value added (current US$), these industrialised countries Footnote 1 are selected. The countries are China, United States, Japan, Germany, South Korea, India, Italy, France, United Kingdom, Mexico, Indonesia, Russia, Brazil, Canada, Spain, Turkey, Thailand, Switzerland, Ireland and Netherland.

• Unbalanced panel data

This is a panel data study covering the data period 1960–2019. Our data are unbalanced due to the unavailability of all data for the entire period for all sample countries. The data for this study are collected from the World Development Indicator [ 6 ] published by the World Bank. The used data for the selected variables are on crude death rate (per 1000 people), CO2 emissions from manufacturing industries and construction (% of total fuel combustion), nitrous oxide emissions (thousand metric tons of CO2 equivalent), gross domestic product (GDP) per capita (constant 2010 US$), physicians (per 1000 people), urban population (% of total population), people using at least basic drinking water services (% of population), people using at least basic sanitation services (% of population) and secondary school enrolment (% of gross).

Theory, data, econometric approach and estimation software

Grossman [ 55 ] introduces the health production function, which explains the link between health input and an individual’s health output. The individual health production function can be explained as below:

where HO indicates an individual’s health output and HI denotes input needed for an individual’s health. The above model investigates individual health outcome at the micro level. We examine the impact of industrial pollution on health status at the macro level. Following Majeed and Ozturk’s [ 56 ] study, we converted the above model to macro level. The health inputs are divided into economic, environmental and social factors ([ 56 , 57 , 58 ], which can be expressed by the below equation:

Adding healthcare factors, we have extended the eq. ( 2 ). Hence, eq. ( 2 ) can be written as follows:

We used two environmental variables that arose from industrial pollution: CO2 emissions from manufacturing industries and construction, and nitrous oxide emissions. We then developed two models using two industrial pollution variables. The first and second models consisted of CO2 emissions and Nitrous oxide emissions, respectively. In addition to environmental factors, we have also added a range of economic, healthcare and social factors in our models: GDP per capita (economic factor), doctor/population ratio, sanitation, drinking water (healthcare facility factors), secondary school enrolment and urbanisation (social factors). Hence, our models for empirical investigation is as follows:

where DEA is our dependent variable that represents the death rate. The right-hand side variables are explanatory variables where CO2, NIT, GDP, PHY, WAT, SAN, SCH and URB denote CO2 emissions, nitrous oxide emissions, GDP per capita, physicians, drinking water services, sanitation services, secondary school enrolment and urbanisation, respectively.

Following previous studies such as those of Majeed and Ozturk [ 56 ] and Siddique and Kiani [ 58 ] among others, we also took the logarithm of our variables. One of the main advantages of taking the logarithm is that coefficient estimates will provide the elasticities directly. Therefore, the models for our empirical study will be as follows:

Heteroscedasticity, serial correlations and cross-sectional dependences generally exist in panel data because of an increasing availability of data, rapid urbanization and industrialisation, improvement of sanitation and water facilities on a priority basis, better education opportunities, positive economic development, significant amount of industrial pollution, focus on public health issues and economic globalization. All these factors are more common in the case of world’s most industrialised countries. Moreover, if both the cross-section dimension (N) and the time series dimension ( T ) are large, countries’ economic development may be mutually dependent. Therefore, ignoring the heteroscedasticity, the serial correlations and the cross-sectional dependences may provide inefficient statistical inference [ 59 ].

The standard fixed effect model will not be able to produce robust results if a panel data set contains heteroscedasticity, autocorrelation, and cross-sectional dependence. Therefore, this study adopts Hoechle’s [ 60 ] procedure of the STATA xtscc program that produces Driscoll and Kraay’s [ 38 ] standard error technique for linear panel models. These are consistent for heteroskedasticity and also robust to general forms of cross-sectional dependence to examine the impact of industrial pollution on health status for a panel of industrial countries. For applying Driscoll and Kraay’s [ 38 ] standard error technique, this study follows a two-steps procedure. The average values obtained from the product of independent variables and residuals is the first step. These values in a weighted heteroskedasticity autocorrelation (HAC) estimator will be used to generate standard errors, which now have the added feature of being robust against cross-sectional dependence in the second step [ 61 , 62 , 63 ]. There are a number of advantages of having Driscoll and Kraay’s [ 38 ] standard error technique. First, it is one of the best techniques if there is any scope of heteroscedasticity, cross-sectional dependency and serial correlation in the data [ 64 , 65 , 66 ]. Second, this technique is a non-parametric approach which accommodates flexibility, and large time dimension. Third, this technique can apply in both balanced and unbalanced panel data. Finally, this technique can handle missing values [ 60 ].

Following the methodology of Le and Nguyen [ 67 ]; Ikpesu et al. [ 68 ] we have also employed the Panel-corrected standard error (PCSE) technique for robustness checking and validating our outcomes.

A series of econometric procedures have been applied to check the unbalanced panel data. First, the study checks the presence of heteroscedasticity, serial correlation, and cross-sectional dependence in the panel data. Modified Wald statistics for groupwise heteroskedasticity will be used to see the existence of heteroscedasticity in the data set [ 69 ]. The presence of serial correlation will be tested using Wooldridge [ 70 ]. Pesaran [ 71 ] CD statistic is a diagnostic test that checks the existence of cross-sectional dependence. Only Pesaran’s CD test is adequate while using unbalanced panels [ 60 ]. Pesaran’s [ 71 ] CD test is given as below:

Where \( {\hat{p_{ij}}}^2 \) represents the pairwise cross-sectional correlation coefficient of residuals, and T and N represent the time and cross-sectional dimensions of the panel, respectively. In this setting, the null hypothesis has cross-sectional independence with CD ~ N (0, 1).

Empirical results

Descriptive statistics.

Table  1 presents the descriptive statistics of the variables. The average (median) value of crude death rate is 9.05 (8.70). The minimum and maximum of crude death rate are 4.69 and 25.43, respectively. The mean and median values of CO2 emissions are 21.80 and 21.16, respectively. The average (median) value of nitrous oxide emissions is 83.65 (38.09). The average of GDP per capita, physicians, urbanisation, drinking water services, sanitation services and school enrolment are 21,267.66, 1.99, 62.42, 96.43, 89.11 and 82.71, respectively.

Results of heteroscedasticity and autocorrelation

Table  2 presents the results of heteroscedasticity and autocorrelation. The presences of heteroscedasticity, serial correlation and cross-sectional dependence in panel data have serious problems for econometric analysis. Heteroscedasticity exists when the variance of the disturbance differs across samples [ 72 ]. Autocorrelation is the error term correlated with any variable of the model which is not affected by the error term related to other variables in this model [ 73 ]. Table 2 ensures the existence of heteroscedasticity and autocorrelation.

Results of cross-sectional dependence test

Table  3 reports Pesaran’s [ 71 ] cross-sectional dependence test results. The presence of cross-sectional dependence in a panel study suggests the existence of common unobserved shock among the cross-sectional variables over a time period [ 74 ]. The results show that the null hypothesis of cross-sectional dependence is rejected at the 1% statistical significance level for all variables used in this study implying that there is strong evidence of the presence of cross-sectional dependence.

Results of Driscoll-Kraay standard error estimation

This study estimates regression results using Hoechle’s [ 60 ] procedure with Driscoll-Kraay’s [ 38 ] robust standard error to validate the statistical inferences. All variables except GDP per capita and urbanization are found to be significant at the 1% level while using Eq. ( 5.1 ) in Model 1 of Table  4 . The GDP per capita and urbanization are significant at the 5% level. Carbon emissions positively and significantly contribute to industrial pollution which leads to an increase in the crude death rate, suggesting that a 1% increase in CO2 emissions increases crude death rate by 0.10% in the world’s twenty most industrialised countries. This result is comparable with that of Siddique and Kiani [ 58 ] who found that a 1% increases in CO2 emissions increases infant mortality rate by 0.14, 0.09 and 0.26% in middle-income, upper-middle-income and lower-middle-income countries, respectively.

The impacts of a number of factors on crude death rate: economic growth, availability of physicians, urbanization, accessible sanitation and education are negative and statistically significant indicating that 1% increase in these factors decreases crude death rate by 0.07, 0.12, 0.13, 0.45 and 0.10%, respectively. Since the average income of workers in industrial countries is high, they are likely to have better resources and technologies to reduce the death rate arising from industrial pollution. The residents from industrialised countries can have more accessibility to doctors and healthcare facilities that reduce the death rate from industrial pollutions. Urbanization, sanitation and education have positive effects on health status [ 58 ] that mitigate the crude death rate. Our obtained results confirm this proposition empirically.

Model 2 of Table 4 shows the results using Eq. ( 5.2 ). The effect of nitrous oxide emissions on crude death rate is positive and statistically significant at the 1% level implying that a 1% increase in of nitrous oxide emissions increases crude death rate by 0.07% in the sample countries. This result is also comparable with that of Siddique and Kiani [ 58 ] who find that a 1% increase in nitrous oxide emissions increases infant mortality rate by 0.21, 0.24 and 0.19% in middle-income, upper-middle-income and lower-middle-income countries, respectively. Economic growth, access to physicians, urbanization and sanitation have a negative and significant effect on the crude death rate suggesting that 1% increase in these areas decreases the crude death rate by 0.08, 0.13, 0.17 and 0.39%, respectively. Our findings of economic growth and sanitation facilities are in line with those of Rahman et al. [ 15 ] and Kengnal and Holyachi [ 75 ], and the effect of access to physicians is consistent with the findings of Shahid et al. [ 76 ]. However, our result in relation to urbanisation is contradictory to the findings of Li et al. [ 77 ]. Surprisingly, we have obtained a positive association between crude death rate and basic drinking water services. This result is unexpected and contradictory to the findings of Majeed and Ozturk [ 56 ] who investigated the relationship between infant mortality and safe drinking water, using a global panel sample for the period 1990–2016, and found a negative relationship between infant mortality rate and safe drinking water.

Robustness check

Panel-corrected standard error (PCSE) technique effectively deals with heteroscedasticity, serial correlations, and cross-sectional dependence [ 67 , 68 ]. Therefore, we use PCSE estimation as robustness test to compare our results. Table  5 reports the results of PCSE.

Carbon emissions, nitrous oxide emissions and water have significant positive effects on crude death, which are consistent with the results of Table 4 . The economic growth, access to physicians, and sanitation have a negative and significant effect on the crude death rate. Overall, the results from the PCSE estimate show consistent results with the results of Driscoll-Kraay’s [ 38 ] robust standard error estimates.

Conclusions and policy implications

The current study explores the link between health status and industrial pollution in the world’s 20 most industrialised countries, controlling for some other variables. Crude death rate is used to represent health status, and CO 2 emissions from manufacturing industries and construction, and nitrous oxide emissions are considered as markers for industrial pollution. Using annual data for 60 years (1960–2019), an unbalanced panel data estimation method is followed where Driscoll and Kraay’s [ 38 ] standard error technique is employed to deal with heteroscedasticity, autocorrelation and cross-sectional dependence problems. The research findings indicate that industrial pollution arising from both variables significantly increases the death rate, while an increase in economic growth, number of physicians, urbanisation, sanitation facilities and access to schooling decreases the death rate. Therefore, minimisation of industrial pollution should be the topmost policy agenda in these countries. All the findings are consistent theoretically, and have empirical implications as well. These outcomes also comply with the policy guidelines of United Nations Development Program (UNDP) and World Health Organization (WHO) in addressing industrial pollution along with other factors to substantially reduce the death rate by 2030 and improve the public health status (SDGs’ target 3.9 of Goal 3, [ 78 , 79 ]). The policy implication of this study is: the mitigation of industrial pollution, considering other pertinent factors, should be addressed appropriately by enunciating effective policies to reduce the human death rate and improve health status in the studied panel countries. The following particular recommendations will be useful in this respect:

Reducing industrial pollution: The reduction of industrial pollution (CO 2 and nitrous oxide emissions) is essential in relation to environmentally friendly initiatives, which can play a role in reducing pollution related diseases, and eventually diminish the death rate. In this regard, effective pollution disposal facilities should be introduced and technology should be developed to convert industrial wastages into fresh materials and polluted smoke into clean air. A complete and wide-ranging policy package on reducing industrial pollution should be formulated and executed.

Sustainable economic development: Sustainable economic development along with environmental considerations is required to make the earth habitable for future generations. In this perspective, green development, green growth, green technology and a pollution free environment are urgently needed to improve the habitat for humans and thus reduce the mortality rate. Thus efficient and inclusive policy initiatives to ensure sustainable development will be essential for improving the health status of people by reducing the death rate.

Increasing physician numbers: Physicians provide better medical services and guidelines for taking proper drugs and medicines leading to cures from various diseases and improving living standards, which both decrease the mortality rate. In this perspective, a concrete policy venture for generating abundant physician numbers and ease access to them to protect human health is essential.

Enhancing access to clean water and sanitation facilities: Wide access to clean water and better sanitation facilities is required to decrease the mortality rate, as contaminated drinking water and unhygienic sanitation may cause an increase in the death rate. A well-thought out and well-accepted policy initiative is required to facilitate access to clean water and sanitation facilities to all people.

Enlarging educational opportunities: Educational facilities increase awareness of medical and health consciousness to protect people from various fatal diseases and therefore reduce the death rate. An effective policy formulation is necessary to enlarge widespread educational facilities among the entire population to reduce the mortality rate.

Well-organized urbanization: Well-planned urban facilities may increase living standards and increase quality of life by establishing well-organized housing, industries, hospitals, supplying electricity, clean water and hygienic sanitation facilities. Therefore, a complete well-organized urbanization policy design is urgently needed in conjunction with other policies.

Availability of data and materials

The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request.

Data source for these countries: World Bank national accounts data, and OECD National Accounts data files

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Rahman, M.M., Alam, K. & Velayutham, E. Is industrial pollution detrimental to public health? Evidence from the world’s most industrialised countries. BMC Public Health 21 , 1175 (2021). https://doi.org/10.1186/s12889-021-11217-6

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Industrial odour pollution and human health: a systematic review and meta-analysis

• Victor Guadalupe-Fernandez 1 , 2 ,
• Manuela De Sario 1 ,
• Simona Vecchi 1 ,
• Lisa Bauleo   ORCID: orcid.org/0000-0002-2738-6180 1 ,
• Paola Michelozzi 1 ,
• Marina Davoli 1 &
• Carla Ancona 1  

Environmental Health volume  20 , Article number:  108 ( 2021 ) Cite this article

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To conduct a systematic review to evaluate the association between residential or occupational short- and long–term exposure to odour pollution from industrial sources and the health status of the exposed population.

The searches were conducted in Medline, EMBASE and Scopus in April 2021. Exposure to an environmental odour from industrial sources in population resident near the source or in workers was considered. We considered outcomes for which there was a biological plausibility, such as wheezing and asthma, cough, headache, nausea and vomiting (primary outcomes). We also included stress-related symptoms and novel outcomes (e.g. mood states). Risk of bias was evaluated using the OHAT tool.

For primary outcomes, when at least 3 studies provided effect estimates by comparing exposed subjects versus not exposed, we pooled the study-specific estimates of odour-related effect using random effects models. Heterogeneity was evaluated with Higgins I 2 .

Thirty studies were eligible for this review, mainly cross-sectional ( n  = 23). Only one study involved school-age children and two studies involved workers. Only five studies reported odour effects on objective laboratory or clinical outcomes. Animal Feeding Operations and waste were the most common industrial sources.

The overall odds ratios in exposed versus not exposed population were 1.15 (95% CI 1.01 to 1.29) for headache (7 studies), 1.09 (95% CI 0.88 to 1.30) for nausea/vomiting (7 studies), and 1.27 (95% CI 1.10 to 1.44) for cough/phlegm (5 studies). Heterogeneity was a moderate concern. Overall, the body of evidence was affected by a definitely high risk of bias in exposure and outcome assessment since most studies used self-reported information.

Conclusions

Findings underline the public health importance of odour pollution for population living nearby industrial odour sources. The limited evidence for most outcomes supports the need for high quality epidemiological studies on the association between odour pollution and its effects on human health.

Peer Review reports

Introduction

Odour emissions from industrial sites constitute a major health issue both for neighbouring residents and workers, mainly due to the olfactive nuisances generated during industrial production processes [ 1 , 2 , 3 ]. Nevertheless, little evidence is available on the impact of olfactory nuisance, compared to a large number of studies on the toxicity of the chemicals emitted by industrial plants such as wastewater treatment, livestock operations, composting facilities, landfills, paper and pulp mills or petrochemical industries. Odour pollution is regulated differently worldwide, and it is addressed at a national or municipal level by different policy frameworks [ 2 , 4 ].

The olfactory function plays an important role in the detection of hazards in the environment, with the upper respiratory tract usually being the first point through which air pollutants enters the human body. Olfactory receptors of the nasal epithelium may detect odorant compounds inducing sensations in different ways. At elevated concentrations, odorant receptors may send signals via the olfactory and trigeminal nerve to the brain causing different reactions, also known as subjective symptoms. Odour sensations processed in the central nervous system may induce pleasant reactions, positive mood and emotions, but also negative responses including irritation, pain, sneezing, salivation, and vasodilation, ultimately resulting in nasal obstruction, bronchoconstriction, mucus secretion and inflammation. Malodours, mould or bad air quality have also been considered as environmental triggers of headaches, eyes irritation, and unusual tiredness [ 3 , 5 , 6 , 7 , 8 , 9 , 10 ]. It is also important to note, that individuals’ sensory responses can vary due to physiological factors, age or sex, persistent exposure, perceived health risk, and various social factors [ 3 , 5 , 6 , 7 , 8 , 9 , 10 , 11 ]. Odour-related symptoms seem more common in subjects with odour intolerance [ 5 ]. In fact, odour seems to not have an effect per se, but it is mediated by personal perception or annoyance [ 7 , 10 ]. Annoyance is a psychological symptom that can be related to poor quality of life or negative mood states.

Several studies measure odour annoyance and monitor community impact by self-reporting of somatic symptoms, as well as objective health effects, commonly including respiratory inflammation and dysfunctions diagnosed by physicians. The population’s characteristics and health status have traditionally been considered in surveys and structured interviews when approaching odour assessment [ 12 ].

Estimations of odour frequency, intensity and hedonic tone in the environment differ substantially among countries, according to their odour regulations [ 1 , 2 , 3 , 4 , 12 ] and there are no standardized methods for population and exposure assessment to be used for environmental epidemiology studies. Odours emissions are generally composed by complex mixtures of different volatile chemical compounds. Besides, the sensitivity of people and odours responses are different among individuals, hindering efforts to monitor and assess its health effects. In view of the above, it is considered that odour analytical tools are not sufficiently accurate [ 1 , 5 , 13 , 14 , 15 ]. However, there are some predictive and observational approaches that have been used to estimate population odour exposure, such as atmospheric dispersion models [ 2 ], distance to the source [ 12 ], frequency of odour events per year, sniff tests [ 1 ], chemical compounds analysis [ 16 ], population complaints monitoring (mean annoyance response or percent highly annoyed residents) [ 3 , 10 ].

As a result, the overall impact on communities of odour emissions remains unclear and there has been a rising number of concerns and complaints regarding their possible health effects, ending up increasing the quantity of studies performed on this topic lately [ 4 , 10 ].

We conducted a systematic review to evaluate the association between residential or occupational short- and long–term exposure to odour pollution from industrial sources and the health status of the exposed population.

Methods/design

Protocol and registration.

Methods and inclusion criteria were registered for PROSPERO (registration number: CRD42018117449). The systematic review was reported according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement guidelines [ 17 ].

Eligibility criteria

Eligibility criteria were defined based on the PECO statement for the key elements (population, exposure, comparator and outcome). The population of interest were people of any age living near industrial sources or workers exposed to odour pollution in their workplace. We limited the definition of an industrial source as all areas hosting production and processing plants and facilities for chemicals, petrochemicals, manufacturing, waste or water disposal and/or treatment, cement, power generation, mining and metals, and we included other activities, such as production in industrial installations of pulp and paper, textile, slaughterhouses and livestock operations. We excluded studies which assessed the effects of exposure to indoor pollution sources. Studies were included if they captured exposure to an environmental odour from industrial sources including both objective and subjective measures. Nevertheless, we excluded studies that mainly were focused on malodorous toxic compounds emissions since it would be difficult to disentangle the odour effect from the toxic one. The comparison group represented any alternative to the exposed group; this was the minimum criterion for inclusion.

We considered primary outcomes for which there was a biological plausibility with the exposure, such as wheezing and asthma, cough, headache, nausea and vomiting. Odour annoyance has been considered both as a surrogate for exposure and outcome, having a strong association with odour intensity, hedonic tone and modelled odour from dispersion models [ 3 ]. We also considered secondary outcomes such as respiratory, stress-related symptoms and other stress-related consequences (e.g. cardiovascular sleep disorders), and also novel outcomes (e.g., mood) [ 5 , 7 , 18 ]. There was no prior restriction on the method used for outcome measurement. We excluded studies based on comparisons between odour exposure and odour discrimination and hedonic ratings. We included both observational and experimental study designs evaluating short- and long–term effects of odour pollution with an estimate health effect.

Information sources and search

A preliminary search was conducted in bibliographic databases to identify subject terms and free terms relevant to the review question. Afterwards we developed a comprehensive systematic search strategy using a combination of Medical Subject Headings (MeSH) terms and free text terms. We revised the strategy appropriately for each database to take account of differences in controlled vocabulary and syntax rules. We implemented our search on April 2021, in Medline (via OVID, 1946 to search date) and EMBASE (1947 to search date). To identify additional studies, we screened the references list of the included studies and searched the related articles publication, through Scopus (2004 to search date). We set no date, and geographiclimits in our search strategy. We searched for grey literature by examining different university libraries, and national/government/NGO reports. Furthermore, we contacted experts seeking additional information about unpublished and published studies. The Ovid search string is presented in Additional file 1 .

Study selection

We uploaded search results into a reference management software (EndNote, Clarivate Analytics) to manage the screening and coding process. Two reviewers independently screened titles and abstracts of the records obtained from the searches (VFG, MDS). The full texts of potentially eligible studies were retrieved for evaluation and inclusion. Any discrepancy regarding inclusion or exclusion of a particular study between reviewers was resolved through discussion by a third reviewer (AC).

Data collection process and data items

For studies that met inclusion criteria, two review authors independently extracted data using a data extraction form. Disagreements about the extracted information were resolved by discussion with the involvement of the research team when necessary. We contacted three authors for further information. All authors responded, one of them provided numerical data that had only been presented graphically in the published article, one provided a digital poster while the one remaining author could not provide the requested information.

Furthermore, the reviewers extracted data on study year and design from each study, sampling time frame, region or country where the study was performed, sample size (target, enrolled, follow-up rates) and characteristics of the population, description of the reference or control group, exposure definition (data sources) and assessment (e.g. distance from the facility, odour annoyance using a 5-point-likert scale or dispersion modelling odour assessment), health outcomes collected (methods used to measure the outcome), statistical approach performed by the authors to analyse the data, confounders or co-exposures (methods used to measure them and how they were considered in analysis), type of effect measure (Risk Ratio, RR; Prevalence Ratio, PR; Odds Ratio, OR; beta coefficients; absolute and relative change) and the 95% confidence interval (CI). When more than one effect measure was available from the same paper, the following sequential but alternative criteria (if the first does not apply, the second works and so on) were applied to choose the estimate to be extracted: that from the best adjusted model; the most significant one; the largest effect size. Information on funding and conflict of interest by the authors of the studies was extracted and considered when available.

Risk of bias assessment in individual studies

The risk of bias (RoB) of included studies were independently assessed by two reviewers. Disagreements were discussed and resolved with a third author by consensus. We used the National Toxicology Program/Office of Health Assessment and Translation (NTP/OHAT) Risk of Bias Rating Tool for Human and Animal studies adapted to the review question (Program) [ 19 , 20 ]. The tool considered nine domains: assessment of exposure, assessment of outcome, confounding (three elements), selection bias, performance bias, attrition/exclusion bias, outcome reporting bias and inappropriate statistical methods as an additional category for other potential threats to internal validity. Assessment of confounding was based on three elements: 1) the design or analysis accounting for confounding and modifying variables, 2) the adjustment for other concurrent exposures 3) the confounding variables measured reliably and consistently. The first two elements were evaluated according to the minimum set of confounders and co-occurring exposures considered a priori as relevant: sex, age, educational level/ socioeconomic status (SES)/ employment status, smoking status (active/passive) and any co-exposures (noise, traffic pollution, air pollution, indoor odour).

According to the OHAT risk-of-bias (RoB) tool, for each specific domain, a risk of bias “definitely low”, “probably low”, “probably high”, and “definitely high” was assigned and each paper was classified accordingly. We classify individual studies into an overall quality category, i.e. tiers from 1 (higher quality) to 3 (lower quality). The entire body of evidence was rated and grouped as having “not likely”, “serious” or “very serious” risk of bias, based on the RoB across studies and classification tiers. Confidence ratings were integrated on a standard evidence profile table.

Data synthesis

Data patterns were explored and evaluated. Outcome-specific odour-related effects were extracted from each study into evidence tables. For primary outcomes, in cases in which at least 3 studies provided effect estimates by comparing exposed subjects versus not exposed, we pooled the study-specific estimates of odour-related effects. Effect estimates using different metrics (e.g. beta coefficients for unit increase in odour or risk ratio across multiple exposure categories) were not included in the meta-analysis. We pooled estimates using random effects models (Restricted Maximum Likelihood REML Method) [ 21 ]. Heterogeneity was evaluated with the I squared statistic [ 22 ], where 25%, 50% and 75% indicate a low, medium, high heterogeneity respectively. To assess if exposure assessment (subjective vs objective) was a potential explanatory factor for the heterogeneity, a stratified analysis was planned. We planned to assess the publication bias only for at least 10 effect estimates.

A narrative synthesis of the results was carried out for secondary outcomes.

Meta-analyses were carried out in STATA software version 14.0.

Our search identified 5770 records after the removal of duplicates. Of these, 5695 were discarded on the basis of title and abstracts. No study was identified from grey literature sources. Seventy-five records were subsequently included in the full-text evaluation. From those, a total of 30 studies were included in the final synthesis with two additional records identified through reference list of the studies (Fig.  1 ).

Systematic review on industrial odour effects on health - PRISMA flow diagram

Figure  2 shows the geographical distribution of the studies by country, with most sudies placed in Europe. Study size ranged from 15 to 58,169 subjects. The majority of the studies had a cross-sectional design ( n  = 23), while seven were panel studies [ 23 , 24 , 25 , 26 , 27 , 28 , 29 ].

Geographic distribution of the included studies on industrial odour effects on health

The characteristics of the included studies, ordered by study design and by publication year (newer to older), are summarized in Table 1 and additional information are reported in Additional files 2 and 3 .

Only one study [ 43 ] involved a sample of school-age children (age range: 12–14 years). We observed a large heterogeneity in terms of type of industrial source, study population, measurements for exposure and outcome (i.e. objective or subjective) and type of outcomes. Regarding industrial source of exposure, 13 studies were conducted on Animal Feeding Operations (AFOs), 10 studies on waste (both solid and liquid waste), 2 were on multiple sites, and 6 were on other industrial exposure (e.g. paper, petrochemical plant).

Ten studies used distance from the source as proxy of odour exposure [ 26 , 30 , 31 , 39 , 40 , 43 , 45 , 47 , 50 , 51 ].

Boers et al. 2016 estimated odour exposure using the Stacks dispersion model [ 34 ]. Lipscomb et al. [ 49 ] defined a measure of exposure based on odour zones adopted from an earlier survey. In addition, Blanes-Vidal [ 37 ] and van Kersen [ 29 ] included NH 3 exposure as a proxy of odour exposure. In one study, two different exposure measures were used, distance and odour frequency measured by a group of trained panellists [ 47 ]. In 16 studies [ 9 , 23 , 24 , 25 , 27 , 28 , 29 , 35 , 37 , 38 , 41 , 42 , 44 , 45 , 47 , 48 ], perceived level of exposure was rated labelling different scales (Likert-type scales and other alternatives) through questionnaires/interviews. Several studies used a dichotomous exposure of odour annoyance and/or odour perception, defined as presence/absence [ 9 , 24 , 29 , 35 , 36 , 39 , 41 , 43 , 45 ] .

Retrospective and self-reported information on outcomes, questionnaire-based, was the most widely used method for measuring primary outcomes. Most studies were related to both acute (e.g. symptoms, worsening of disease) and chronic outcomes (e.g. prevalence of diseases), with different timing of data collection, with past year prevalence in some studies [ 30 , 36 , 39 , 43 , 45 , 49 ] or past 2 years [ 37 , 40 ], or past 6 months prevalence [ 38 ], past 1 month [ 32 , 33 , 37 ], or current symptoms [ 9 , 29 , 31 , 34 , 42 , 43 , 45 , 47 ].

On the contrary, the seven panel studies focused on short-term or acute outcomes, that varied on a daily base, such as symptoms of disease [ 24 , 27 ], or mood [ 25 , 26 ] or biological parameters such as lung/bronchial function [ 27 , 29 ], immune function and allergy [ 23 ], blood pressure [ 28 ]. In addition, also a cross-sectional study [ 42 ] reported objective outcomes (bronchial hyperresponsiveness to methacholine, IgE concentration). In some studies information on timing of outcome data collection was not provided [ 9 , 46 , 47 , 48 , 50 , 51 ].

Most cross-sectional studies took into account the potential confounding of age, sex, smoking status, educational level and/or SES [ 32 , 33 , 35 , 36 , 37 , 38 , 39 , 41 , 42 , 43 , 44 , 45 ]. Panel studies [ 23 , 24 , 25 , 26 , 27 , 28 , 29 ] were adjusted only by time-varying variables (e.g. time of the day when outcome was measured) because they do not need to adjust for individual confounders since the study population serves as its own control. Eight studies [ 9 , 26 , 30 , 46 , 47 , 49 , 50 , 51 ] did not account for any confounder and only one [ 30 ] reported to have matched exposed and control population by age, race and education level. One study on COPD patients restricted the study population to non-smokers [ 29 ].

Figure  3 shows the results of evaluation of the risk of bias of the studies selected for the review. Overall, the body of evidence was affected by a definitely high risk of bias in exposure and outcome assessment since most studies used self-reported information. The study from Steinheider 1998 has been evaluated separately for the two study sites (Norvenich study labelled as a) and Nettetal study labelled as b)) [ 47 ]. Sixteen studies were classified in the worst quality level (3rd tier), 10 studies in the second (2nd tier) and five studies in the first category (1st tier).

Studies on industrial odour effects on health according to the NTP/OHAT risk of bias approach. * conference proceeding; **Steinheider et al. 1998a Nörvenich study, Steinheider et al. 1998b Nettetal study

Confidence in exposure and outcome assessment was very low in most studies. Only three studies were judged at low risk of bias since used objective outcome measures or only exposure from dispersion models [ 23 , 28 , 34 ].

As for confounding, adjustment with a minimum set of potential confounders was achieved in most studies for which the risk of bias was labelled low; 11 studies that did not account for any confounders were graded as “probably high” or “definitely high” risk of bias [ 9 , 26 , 30 , 31 , 34 , 40 , 46 , 47 , 48 , 49 , 50 , 51 ]. The second confounding element referred to the adjustment of other environmental exposure and in this case most studies did not adjust for concurrent exposures. For example, panel studies that only accounted for time of day (morning /evening) were considered as “probably high RoB” [ 23 , 24 , 28 ], due to the lack of adjustment for time-varying air pollution or noise. The third confounding element regarding validity and reliability of measures was characterized by a high risk of bias in most studies since information was mostly self-reported. Eight studies accounted for potential co-exposures, such as smoking, noise, indoor and/or outdoor pollution and were judged at very low/low risk of bias [ 24 , 25 , 27 , 35 , 38 , 40 , 41 , 43 ].

The risk of selection bias resulted to be definitely high in five studies because the control group could not be defined as truly unexposed [ 31 , 38 , 41 , 46 , 49 ] or because personal attitude towards livestock farming could have influenced participation [ 29 ]. The risk of selection bias was probably high in most studies. Additionally, in six studies [ 32 , 33 , 34 , 35 , 43 , 44 ] and in the two Steinheider’s study sites [ 47 ] no information was provided as to whether selection of study participants resulted in appropriate comparison groups (Fig.  3 ). Regarding the attrition bias, in 10 studies [ 25 , 26 , 32 , 33 , 36 , 40 , 45 , 46 , 48 , 49 ] and in the two Steinheider’s study sites [ 47 ] the information about loss of participants was unclear or incomplete, hence they were considered at “probably high” risk of attrition bias. Missing values related to outcome variables in the study were treated in the analysis. Only three studies were classified at “definitely low risk” of attrition bias [ 23 , 28 , 39 ]. Six studies were judged at probably or definitely high risk of reporting bias [ 26 , 29 , 30 , 31 , 39 , 40 ], and, additionally, two studies [ 36 , 46 ] were at unclear risk since outcomes were not reported with sufficient detail in the short communications. A probably low risk of reporting bias was found in Sucker et al. [ 41 ], after evaluating a previous publication of another part of the results [ 52 ].

Regarding the additional element of appropriate statistical methods, nine studies were judged at high risk (probably or definitely) since they provided only a descriptive analysis [ 9 , 26 , 31 , 42 , 44 , 46 , 49 , 50 , 51 ] and in the two Steinheider’s study sites [ 47 ].

Health outcomes were grouped as follows (Additional file 2 ): general ill feelings (e.g. headache, sleeping problems), gastrointestinal symptoms (e.g. nausea/vomiting, reflux), lower and upper respiratory symptoms (e.g. cough/phlegm, wheezing), immune function/allergy mucus irritation, skin disorders, mood states, cardiovascular problems, and odour nuisances (e.g. odour annoyance, risk perception). We ran meta-analyses for headache, nausea/vomiting and cough/phlegm. The Additional file 3 reported also the results not included in the meta-analyses of the association between residential or occupational, short- and long–term exposure to odour pollution from industrial sources and the risk. No measure of association was available for five studies [ 9 , 30 , 46 , 50 , 51 ] and for one of the locations (Nettetal) studied in Steinheider [ 47 ]. Only graphical results of Odds Ratios (and 95% confidence intervals) were provided for the association between NH 3 exposure and prevalence of symptoms in the study of van Kersen 2020 [ 29 ].

Nineteen studies analysed general ill symptoms as health outcome of odour related effects [ 9 , 24 , 27 , 30 , 32 , 33 , 35 , 37 , 38 , 39 , 40 , 41 , 44 , 45 , 46 , 47 , 49 , 50 , 51 ] (Additional file 3 ). All studies were on adults. Two studies were conducted among workers [ 32 , 33 ].

Headache was the most common general ill symptom, being reported in 16 studies. Pooled analysis showed an increased risk of headache in exposed versus not exposed (OR = 1.15, 95% CI: 1.01 to 1.29) with moderate heterogeneity (I 2  = 66%, p -value = 0.004) (Fig.  4 ). Among studies that were not included in the meta-analysis (Additional file 3 ), one study showed increasing headache prevalence [ 47 ] and two studies [ 37 , 45 ] showed increasing risk in the highest exposure categories: at extremely annoyed compared to those who were not annoyed (OR = 3.65; 95% CI: 1.27 to 10.5); odour intolerant vs tolerant (OR = 2.64; 95% CI 2 to 3.5); group with complaints with impacts on health vs no complaint group (OR = 2.04; 95% CI 1.46 to 2.84).

Forest plot of study-specific and pooled Odds Ratio (OR) and 95% Confidence Intervals (95%CI) of residential exposure to odour and headache in exposed versus non exposed subjects

Ten studies evaluated exposure to odour objectively [ 30 , 32 , 37 , 39 , 40 , 45 , 47 , 49 , 50 , 51 ], reporting sparse evidence of association for dizziness [ 40 ], sleeping difficulties [ 47 ], fatigue [ 49 ], joint pain [ 39 ], fever past 12 months [ 39 ] and toothache [ 49 ].

Among studies evaluating exposure subjectively [ 9 , 24 , 27 , 35 , 37 , 38 , 39 , 45 , 51 ], most consistent associations were found for dizziness [ 24 , 35 , 37 , 45 ], unnatural fatigue [ 37 , 39 , 45 ] and joint/muscular pain [ 39 , 45 ].

Among exposed workers, significant higher total subjective health complaint (SHC) score [ 53 ] and the subjective neurological complaints score were found in exposed workers than in controls and these associations lasted for at least 3 years after the pollution was removed [ 32 , 33 ].

Fifteen studies reported gastrointestinal symptoms [ 9 , 24 , 27 , 30 , 32 , 35 , 37 , 38 , 39 , 40 , 45 , 47 , 49 , 50 , 51 ]. All studies were on adults. Only one study included workers [ 32 ].

The most frequent gastric symptom reported was nausea/vomiting. Seven studies [ 9 , 24 , 35 , 38 , 39 , 40 , 49 ] were feasible to meta-analysis (Fig.  5 ), showing an increased risk of these symptoms (OR = 1.09; 95% CI: 0.88 to 1.30) with a low heterogeneity (I 2  = 28.3%; p -value = 0.193). Among studies not included in the meta-analysis (Additional file 3 ), self-reporting of vomiting, nausea or retching was significantly higher for increase in odour frequency in Nörvenich site [ 47 ] and in the study of Segala et al. [ 45 ] in the highest exposure categories: odour intolerant vs tolerant (OR = 3.52; 95% CI 2.14 to 5.8) and in group with complaints with impacts on health vs no complaint group (OR = 2.11; 95% CI 1.13 to 3.94). Estimates of the odour-nausea association tended to increase as the level of odour annoyance increased, but results were not significant in Blanes-Vidal et al. [ 37 ].

Forest plot of study-specific and pooled Odds Ratio (OR) and 95% Confidence Intervals (95%CI) of residential exposure to odour and nausea/vomiting in exposed versus non exposed subjects

Among other gastric symptoms, eight studies measured exposure objectively [ 32 , 39 , 40 , 45 , 47 , 49 , 50 , 51 ]. High exposure to odours was associated with greater prevalence of loss of appetite (OR = 4.27; 95% CI: 1.43 to 12.73) [ 49 ]. One study [ 47 ] showed a higher frequency of gastric symptoms (disgust, loss of appetite, stomach discomfort) when the frequency of odour exposure was increased. Another study [ 51 ] reported a significant trend by area among women who had reported frequently or occasionally constipation.

Seven studies evaluated exposure subjectively [ 24 , 27 , 35 , 38 , 39 , 45 , 51 ]. Segala et al. [ 45 ] reported more frequent diarrhoea in people with self-reported odour intolerance (OR = 2.18, 95% CI: 1.43 to 3.33) or experiencing malodour-related health complaints (OR = 2.83, 95% CI: 1.82 to 4.4); however, the same study did not report any significant association in people with complaints that were not related to health (OR = 1.08, 95% CI: 0.74–1.58). Aatamila et al. [ 39 ] found an increased risk of diarrhoea in the group with odour perception (OR = 1.3, 95% CI: 1 to 1.7) and with odour annoyance (OR = 1.2, 95% CI: 0.9 to 1.7). Statistically significant associations with stomach pain, gastrointestinal symptoms and constipation were reported in Hooiveld et al. [ 35 ].

There were no observed differences between groups for the gastrointestinal score among workers were observed [ 32 ].

Sixteen studies reported the association of lower respiratory symptoms with odour pollution [ 24 , 27 , 29 , 30 , 35 , 36 , 38 , 39 , 40 , 42 , 43 , 45 , 47 , 49 , 50 , 51 ]. All studies were on adults except one [ 43 ]. No study was conducted on workers.

Eleven studies reported cough and phlegm as odour-related symptoms [ 24 , 27 , 30 , 35 , 36 , 38 , 39 , 45 , 47 , 50 , 51 ]. Pooled analysis showed an Odds Ratio of 1.27 (95% CI: 1.10 to 1.44) (see Fig.  6 ), with moderate heterogeneity (I 2  = 53.8%, p -value = 0.043). Among studies that were not included in the meta-analysis (Additional file 3 ), self-reporting of cough/phlegm was significantly higher in the study of Segala et al. [ 45 ] in the highest exposure categories: odour intolerant vs tolerant (OR = 2.35; 95% CI 1.75 to 3.15) and in the group with complaints with impacts on health vs. no complaints (OR = 1.64; 95% CI 1.15 to 2.32) and in Aatamila et al. [ 39 ] the group of residents living closer to the waste site (distance< 1.5 km: OR = 1.3; 95% CI 1 to 1.8). Cough was significantly associated with odour frequency and even with odour annoyance after adjustment for odour frequency; however, no direct link was revealed between lower respiratory complaints and odour frequency after adjustment for odour annoyance [ 47 ]. Increasing reports of cough in the past 12 h related to 12-h mean odour were found in Schinasi et al. [ 27 ].

Forest plot of study-specific and pooled Odds Ratio (OR) and 95% Confidence Intervals (95%CI) of residential exposure to odour and lower respiratory symptoms

Among other respiratory symptoms, 10 studies reported exposure objectively [ 29 , 30 , 39 , 40 , 43 , 45 , 47 , 49 , 50 , 51 ], mainly with distance as a proxy of exposure. Only three studies reported significant findings [ 43 , 47 , 49 ] for wheezing, asthma and shortness of breath. Mirabelli et al. [ 43 ] found school proximity within 3 miles of a swine CAFO was related to higher physician-diagnosed asthma (PR = 1.07; 95% CI: 1.01 to 1.14, mostly in non-allergic adolescents PR = 1.14; 95% CI: 1.01 to 1.26), asthma medication use (PR = 1.07; 95% CI: 1.00 to 1.15), asthma-related visit to a physician or an emergency department or hospitalization (PR = 1.06; 95% CI: 1.00 to 1.12), while for wheezing no clear association was found (Additional file 3 ) [ 43 ].

Between studies evaluating exposure subjectively [ 24 , 27 , 29 , 35 , 36 , 38 , 39 , 42 , 43 , 45 , 49 , 51 ], eight reported significant health effects [ 27 , 35 , 36 , 38 , 39 , 42 , 43 , 45 ]. Most consistent estimates were reported for asthma [ 36 , 42 , 45 ], while associations with wheezing were weaker. Wing et al. [ 38 ] showed odour from livestock facilities was significant related to difficulty breathing (PR = 1.52, 95% CI: 1.02 to 2.27) and increased the lower respiratory diseases score (mean difference = 0.28, 95% CI: 0.05 to 0.5) for moderate/strong/very strong odour group. According to Segala et al. [ 45 ], people complaining odour intolerance had a higher prevalence of self-reported respiratory infections (OR = 4.81, 95% CI: 3.24 to 7.14) or COPD (OR = 2.95, 95% CI: 1.84 to 4.73), and similar findings were found for the group with complaints with impacts on health vs. no complaints for COPD (OR = 2.05; 95% CI 1.21 to 3.49). People complaining about odours in terms of a health threat are found to be at a higher risk of enduring cough and COPD. Nonetheless, the precision of the effect estimate is lower in this sense. The included studies showed no association between odour and chest pain in the included studies.

Only three studies evaluated lung function and bronchial hyperresponsiveness [ 27 , 29 , 42 ]. A reduction in PEF and FEV1 with increasing odour was suggested in all studies [ 27 , 42 ], however, 95% CIs included the null value, except than for the association between evening PEF (lag 0) and odour annoyance in the van Kersen study [ 29 ]. In addition, no associations were seen between self-reported odour annoyance and bronchial hyper-responsiveness to methacholine [ 42 ].

Eleven studies [ 24 , 27 , 29 , 32 , 35 , 38 , 39 , 45 , 49 , 50 , 51 ] presented data regarding associations between odours and upper respiratory symptoms (Additional file 3 ). All studies were on adults. Only one study was conducted on workers [ 32 ].

Regarding studies with objective exposure [ 29 , 32 , 39 , 45 , 49 , 50 , 51 ], no consistent associations were found between distance zones/exposure to NH 3 and frequency of cold/flu, runny nose, nasal congestion and non-allergic rhinitis [ 29 , 39 , 45 , 49 , 50 , 51 ].

Regarding studies with subjective exposure [ 24 , 27 , 35 , 38 , 39 , 45 , 51 ], a significant effect of odour with an increased risk for runny nose was found in only three [ 24 , 27 , 45 ]. In Segala et al. [ 45 ] the higher risk was found both in people with self-reported chemical intolerance (OR = 2.1, 95% CI: 1.59 to 2.78) and in people complaining of malodour in terms of a health threat (OR = 1.69, 95% CI: 1.22 to 2.32). A border line association was between cold/flu in last month and odour annoyance [ 35 ] (OR = 1.38, 95% CI: 0.97 to 1.99).

In the only study conducted on workers, there were no significant differences between the flu score in exposed subjects and the control group [ 32 ].

Five studies evaluated the effect of odour on the immune system and allergic sensitization by estimating IgE and IgA concentration and an allergy score obtained by questionnaires, using self-reported exposure [ 23 , 42 ] or objective exposure [ 32 , 46 , 49 ], but no association with increasing odour exposure emerged.

Twelve studies evaluated odour effect on mucous membrane irritation [ 9 , 24 , 27 , 30 , 35 , 38 , 39 , 41 , 45 , 49 , 50 , 51 ] (Additional file 3 ). Six studies were conducted on skin disorders [ 24 , 27 , 38 , 39 , 40 , 49 ]. All studies were on adults. No study was conducted on workers.

The symptoms considered in the studies were: eye irritation, sore throat/burning throat, nose irritation, general irritation symptoms, skin irritation/itchy eczema.

Six studies evaluated the occurrence of irritation symptoms objectively by distance zones [ 30 , 39 , 40 , 45 , 49 , 50 ]. Odour effects were found related to prevalence of dry throat within the last 12 months [ 39 , 49 ], nose irritation [ 39 ], and skin irritation [ 49 ].

Regarding studies with subjective exposure [ 9 , 24 , 27 , 35 , 38 , 39 , 41 , 45 , 51 ], significant findings were found for eye irritation/burning eye [ 9 , 24 , 27 , 39 , 45 ] and for sore throat/dry throat/burning throat in five studies [ 9 , 24 , 27 , 39 , 45 ] (both odour tolerance and perception), for nose irritation/burning nose in two studies [ 24 , 27 ], for nose/eye irritation symptoms in one study [ 41 ], and for skin irritation/rash in three studies [ 24 , 27 , 38 ].

Thirteen studies considered that malodour may have an impact on mood [ 24 , 25 , 31 , 33 , 35 , 37 , 40 , 44 , 46 , 47 , 49 , 50 , 51 ]. All studies were on adults. One study was on workers [ 33 ].

Six studies evaluated exposure objectively [ 37 , 40 , 46 , 47 , 49 , 50 ]. Significant associations were only reported for nervousness, and difficulty concentrating [ 49 ].

Nine studies evaluated exposure subjectively [ 24 , 25 , 31 , 33 , 35 , 37 , 44 , 47 , 51 ]. Significant associations were found for all mood outcomes in Horton et al. [ 25 ], for nervousness, angriness, stress, unhappiness in Heaney et al. [ 24 ], and for sadness and stress-related symptoms in Hooiveld et al. [ 35 ]. In Blanes-Vidal et al. [ 37 ], a dose-response association between odour annoyance and difficulty concentration was found.

Considering the study on workers, participants in the high odour score group reported a higher post-traumatic score than those in the low odour score group, and these associations lasted for at least 3 years after the pollution was removed [ 33 ].

Three studies evaluated the effects of odour on cardiovascular symptoms and blood pressure [ 28 , 40 , 45 ]. Each unit of odour increase on an 8-point scale was associated with increases in diastolic blood pressure (mmHg) (OR = 1.26; 95%CI: 1.08 to 1.47), but not in systolic blood pressure [ 28 ]. No significant association was found in the other two studies [ 40 , 45 ].

Ten papers [ 9 , 25 , 30 , 34 , 37 , 41 , 47 , 49 , 50 , 51 ] investigated odour nuisances in the population regarding to their proximity to industries, odour perception, odour frequency or intensity, hedonic tone and NH 3 exposure. All studies were on adults. No study was carried out on workers.

Regarding studies evaluating exposure objectively [ 30 , 34 , 37 , 47 , 49 , 50 , 51 ], odour annoyance showed a significant association with odour frequency [ 47 ], with NH 3 concentration [ 37 ], as well as, with modelled odour exposure [ 34 ]. Moreover, three other studies showed a significant increase in odour nuisances in the closest areas to the odour source [ 30 , 49 , 50 ].

Regarding studies evaluating exposure subjectively [ 9 , 25 , 41 ], a significant dose–response association with odour annoyance was found in Sucker et al. [ 41 ], consistent across the different exposure measure (odour frequency, intensity, hedonic tone), aggravating the effect in subjects severely annoyed, and also in Horton et al. [ 25 ], the latter association was consistent across odour sources (livestock housings, slurry and manure, livestock farming in general).

This systematic review provides the state-of-art on the health effects of odour from industrial sources. Meta-analysis results showed that residential odour exposure was associated to an increased risk of headache and cough/phlegm, and to a borderline risk of nausea and vomiting. We found suggestive associations for the other outcomes investigated (e.g. asthma, mucus irritation, mood states) but evidence is sparse. Only two studies were carried out on occupational setting and they showed a statistically significant higher score of subjective complaints, neurological complaints and post-traumatic stress symptoms in exposed workers than in controls, and these associations persisted at least 3 years after the pollution was removed [ 32 , 33 ].

The associations with headache, cough/phlegm and nausea/vomiting have a biological plausibility. Unpleasant odours are able to modulate autonomic system responses, such as vagal nerve inducing nausea or vomiting [ 5 ]. Another mechanism involves stress, consequent to environmental worry [ 18 ], and stress-related psychosomatic reactions such as chronic muscular tension, headaches, sleep disturbance. Chemicals responsible for odour may cause irritation, supporting the higher risk for cough/phlegm. Eye and nose irritation and asthma exacerbations can also be related to this odour-related irritation but only limited evidence was found in this review. Our review confirms the strong association between odour and annoyance confirming the potential mediation role on odour-related effects. We could not find any information on potential individual effect modifiers such as age, sex, educational level [ 54 ].

So far, only one other systematic review is available focused only on exposure from Animal Feeding Operation proximity providing little evidence of association between surrogate clinical outcomes and respiratory tract-related outcomes [ 55 ]. There is growing public attention on the topic at an international level as documented by the non-negligible number of studies retrieved in this review. Nowadays, there is also an effort by a variety of countries to classify odour as an atmospheric pollutant and regulate emissions by different policy frameworks worldwide [ 4 ].

Some limitations of our review should be mentioned. Formal test for publication bias was not carried out due to the limited number of studies included in the meta-analysis, but we cannot exclude this kind of bias and possibly other related biases (eg, language bias, citation bias, multiple publication bias) [ 56 ]. However, we expect that the comprehensive literature search, including grey literature, may have limited the impact of publications bias. The inclusion of small studies (less than 100 subjects) in our review suggests this bias is not a main concern. Meta-analytical estimates are affected by a moderate degree of heterogeneity due to difference among studies in terms of sources of exposure, population characteristics, study length. An additional concern derives from the multiple hypothesis testing that increases the probability of false positive results due to the multiplicity phenomenon as suggested also by other authors [ 55 ].

Moreover, the associations between odour and headache, nausea or cough need to be considered with caution due to the overall low quality of the studies for methodological problems of the observational study design.

Most of included studies had a cross-sectional design that can only provide a first hint of a hypothesized cause of a disease, but not a proof of causality [ 57 ]. Six studies used a panel approach, commonly used in air pollution epidemiology [ 58 ], representing one of the best options to study short-term health effects of odour although they can be affected by the drop-out bias and limited statistical power.

We used the approach proposed by the US National Toxicology Program [ 19 , 20 ], one of the emerging approaches in the environmental (and occupational) health context, to evaluate the risk of bias of the body of evidence. Overall, 15 out of the 29 studies had a high risk of bias due to the limited confounding control, and exposure and outcome misclassification since most studies used self-reported information. On the contrary, five studies were at low risk of bias and the remaining nine showed an intermediate risk.

Regarding confounding, two aspects are worth of noting. In the present review, the most prevalent sources of odour were animal feeding operations and waste treatment sites. Therefore, exposure to air pollution from these industrial activities can be common and adjustment for concurrent environmental exposures is crucial to disentangle odour-related effects. Only few studies adjusted for these concurrent exposures such as noise, traffic, PM10, bioaerosol, pesticides [ 29 , 35 , 38 , 41 , 43 ], while another one stratified the study population to isolate the odour-only exposed group [ 40 ]. One of the included panel studies, without proper adjustment for concurrent environmental exposures, was downgraded to a high risk of bias [ 26 ]. Another issue emerging from the review is that in many included studies, confounders and co-occurring exposures were assessed by self-report.

Subjective exposure measures, such as odour rating and scores provided by participants, were used in most studies. Self-reported exposure is well known to be affected by information bias. The European Standard procedure for the measurement of odour concentration uses a dynamic olfactometry assessed by a panel [ 59 ]. However, none of the studies adopted this measurement method, but two studies followed other systematic standard methods for the assessment of odour frequency through panellist testing and olfactometers [ 41 , 47 ]. However, it should be considered that the methods for assessing odour exposure should include also individual perceptions as effect modifier on odour impact on a population [ 12 ]. Odour perception, intolerance or annoyance or complaint [ 9 , 35 , 39 , 40 , 45 ] are adequate indicators to this aim. Some of the included studies have used distance as a proxy of odour exposure [ 30 , 39 , 40 , 43 , 45 , 50 , 51 ] and the Nettetal site studied in Steinheider et al. [ 47 ]. In our results, no consistent evidence of effects in the reporting of somatic symptoms was found by distance to the source of exposure. However, the bias should be non-differential across outcomes leading in some cases to underestimate true associations. Another exposure measure was the ammonia concentration in air [ 29 , 37 ]. Although elevated levels of ammonia may cause irritative symptoms [ 60 ], the levels considered in the studies are several orders of magnitude lower than exposure limit in the workplace, 35 ppm for a short-term (15-min) exposure limit in the workplace, about 3000 times higher than the maximum level reported in Blanes-Vidal [ 37 ] and 2 hundred times higher than maximum reported in van Kersen et al. [ 29 ]. However, due to the complexity of odour mixtures, the use of ammonia as a surrogate for odour pollution, as clearly stated by the authors, represents a great limitation [ 37 ].

Included studies discussed the importance of using a standard objective method for exposure and outcome assessment in environmental epidemiology [ 12 , 33 , 34 , 37 , 41 , 42 ], and some authors regarding other exposures mentioned dispersion modelling as a way out of this methodological issue [ 61 ]. Boers et al. was the only study that used air dispersion modelling as proxy of exposure [ 34 ]. Dispersion models include spatial characteristics (e.g. emissions, local meteorological conditions or topographical features, temperature, wind) which play a significant role in determining dispersion, concentration and intensity [ 61 ].

Only 5 out of 30 studies used objective outcome measurements such as lung/bronchial function [ 27 , 29 ], immune function and allergy [ 23 ], blood pressure [ 28 ], bronchial hyperresponsiveness to methacholine [ 42 ]. Most studies lacked medical objective assessments and generally depended on participants recall of symptoms over different time periods that usually go from weeks to over the last 12 months. If in the same study, both outcome and exposure were self-reported, it may have occurred that exposed subjects, experiencing unpleasant odours, were also more worried about their health and therefore more prone to the reporting of health symptoms than non-exposed subjects, creating the case for differential misclassification of the outcome. Some studies tried to reduce this bias by not mentioning odour when presenting the survey or by the use of memory aids to help remember symptoms [ 38 , 39 ]. In addition, respondents may be more likely to recall recent symptoms, also known as seasonal bias, having difficulty in remembering past events, related to the amount of time that has elapsed [ 30 ]. Response bias is a concern in most included surveys, both in terms of low participation rates and missing data to specific questions. That is why, future studies should attempt to address this issue by ensuring adequate response rates to the study or by controlling for non-response e.g. by weighting methods [ 62 ].

A recent European study collected all laws and regulations in efforts toward the management of odour impact in the communities, finding a heterogeneous picture (EU Project D-NOSES). Europe has included odours in the European Directive on industrial emissions (Directive 2010/75/EU) but at national level, laws and environmental guidelines are in place only in some countries such as Italy (Legislative Decree 152/2006). However, no specific public-health guidance is available. Wider considerations of odour exposure are expected to increase with increasing urbanization [ 12 ], e.g., due to waste disposal sites or intensive farming. It is clear that the effective prevention and response to protect public health is a matter of urgency. Addressing the odour problem is also an equity issue, since neighbouring residents of odour-polluted sites are most likely low-income groups, as it happens for air pollution [ 63 ].

Findings from this systematic review underline the public health importance of odour pollution for population living nearby industrial odour sources. The limited evidence for most outcomes supports the need for high quality epidemiological research to better understand the association between odour pollution and its effects on human health. Exposure assessment is crucial and should be improved to overcome the lack of an objective and standardized method. Due to the strong mediation by odour annoyance and lack of evidence on individual effect modifiers, new studies should include also these aspects, for example studying vulnerable groups, such as children or pregnant women, and workers.

Considering the growing efforts in regulating odour pollution, it is important to define standardized methods to estimate its effects on population health, and to provide evidence-based guidance to bridge the gap also from a public health perspective.

Availability of data and materials

The datasets used and/or analyzed during the current study are available as Additional file 3 .

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Authors would like to thank Zuzana Mitrova for her advices for the bibliographic search.

The work was partially fund by the project “Italian Environment and Health Network (RIAS)” – https://rias.epiprev.it/ .

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Guadalupe-Fernandez, V., De Sario, M., Vecchi, S. et al. Industrial odour pollution and human health: a systematic review and meta-analysis. Environ Health 20 , 108 (2021). https://doi.org/10.1186/s12940-021-00774-3

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Is industrial pollution detrimental to public health? Evidence from the world's most industrialised countries

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• 1 School of Business, University of Southern Queensland, Toowoomba, QLD, 4350, Australia.
• 2 Department of Economics, Bangabandhu Sheikh Mujibur Rahman Science and Technology University, Gopalganj, 8100, Bangladesh. [email protected].
• PMID: 34144705
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• DOI: 10.1186/s12889-021-11217-6

Background: Industrial pollution is considered to be a detrimental factor for human health. This study, therefore, explores the link between health status and industrial pollution for the top 20 industrialised countries of the world.

Methods: Crude death rate is used to represent health status and CO 2 emissions from manufacturing industries and construction, and nitrous oxide emissions are considered to be indicators of industrial pollution. Using annual data of 60 years (1960-2019), an unbalanced panel data estimation method is followed where (Driscoll, J. C. et al. Rev Econ Stat, 80, 549-560, 1998) standard error technique is employed to deal with heteroscedasticity, autocorrelation and cross-sectional dependence problems.

Results: The research findings indicate that industrial pollution arising from both variables has a detrimental impact on human health and significantly increases the death rate, while an increase in economic growth, number of physicians, urbanisation, sanitation facilities and schooling decreases the death rate.

Conclusions: Therefore, minimisation of industrial pollution should be the topmost policy agenda in these countries. All the findings are consistent theoretically, and have empirical implications as well. The policy implication of this study is that the mitigation of industrial pollution, considering other pertinent factors, should be addressed appropriately by enunciating effective policies to reduce the human death rate and improve health status in the studied panel countries.

Keywords: Driscoll and Kraay’s standard error; Health status; Industrial pollution; Industrialised countries; Unbalanced panel data.

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4 School of Social and Political Sciences, University of Glasgow, Glasgow, United Kingdom

Eugenia Bezirtzoglou

One of our era's greatest scourges is air pollution, on account not only of its impact on climate change but also its impact on public and individual health due to increasing morbidity and mortality. There are many pollutants that are major factors in disease in humans. Among them, Particulate Matter (PM), particles of variable but very small diameter, penetrate the respiratory system via inhalation, causing respiratory and cardiovascular diseases, reproductive and central nervous system dysfunctions, and cancer. Despite the fact that ozone in the stratosphere plays a protective role against ultraviolet irradiation, it is harmful when in high concentration at ground level, also affecting the respiratory and cardiovascular system. Furthermore, nitrogen oxide, sulfur dioxide, Volatile Organic Compounds (VOCs), dioxins, and polycyclic aromatic hydrocarbons (PAHs) are all considered air pollutants that are harmful to humans. Carbon monoxide can even provoke direct poisoning when breathed in at high levels. Heavy metals such as lead, when absorbed into the human body, can lead to direct poisoning or chronic intoxication, depending on exposure. Diseases occurring from the aforementioned substances include principally respiratory problems such as Chronic Obstructive Pulmonary Disease (COPD), asthma, bronchiolitis, and also lung cancer, cardiovascular events, central nervous system dysfunctions, and cutaneous diseases. Last but not least, climate change resulting from environmental pollution affects the geographical distribution of many infectious diseases, as do natural disasters. The only way to tackle this problem is through public awareness coupled with a multidisciplinary approach by scientific experts; national and international organizations must address the emergence of this threat and propose sustainable solutions.

Approach to the Problem

The interactions between humans and their physical surroundings have been extensively studied, as multiple human activities influence the environment. The environment is a coupling of the biotic (living organisms and microorganisms) and the abiotic (hydrosphere, lithosphere, and atmosphere).

Pollution is defined as the introduction into the environment of substances harmful to humans and other living organisms. Pollutants are harmful solids, liquids, or gases produced in higher than usual concentrations that reduce the quality of our environment.

Human activities have an adverse effect on the environment by polluting the water we drink, the air we breathe, and the soil in which plants grow. Although the industrial revolution was a great success in terms of technology, society, and the provision of multiple services, it also introduced the production of huge quantities of pollutants emitted into the air that are harmful to human health. Without any doubt, the global environmental pollution is considered an international public health issue with multiple facets. Social, economic, and legislative concerns and lifestyle habits are related to this major problem. Clearly, urbanization and industrialization are reaching unprecedented and upsetting proportions worldwide in our era. Anthropogenic air pollution is one of the biggest public health hazards worldwide, given that it accounts for about 9 million deaths per year ( 1 ).

Without a doubt, all of the aforementioned are closely associated with climate change, and in the event of danger, the consequences can be severe for mankind ( 2 ). Climate changes and the effects of global planetary warming seriously affect multiple ecosystems, causing problems such as food safety issues, ice and iceberg melting, animal extinction, and damage to plants ( 3 , 4 ).

Air pollution has various health effects. The health of susceptible and sensitive individuals can be impacted even on low air pollution days. Short-term exposure to air pollutants is closely related to COPD (Chronic Obstructive Pulmonary Disease), cough, shortness of breath, wheezing, asthma, respiratory disease, and high rates of hospitalization (a measurement of morbidity).

The long-term effects associated with air pollution are chronic asthma, pulmonary insufficiency, cardiovascular diseases, and cardiovascular mortality. According to a Swedish cohort study, diabetes seems to be induced after long-term air pollution exposure ( 5 ). Moreover, air pollution seems to have various malign health effects in early human life, such as respiratory, cardiovascular, mental, and perinatal disorders ( 3 ), leading to infant mortality or chronic disease in adult age ( 6 ).

National reports have mentioned the increased risk of morbidity and mortality ( 1 ). These studies were conducted in many places around the world and show a correlation between daily ranges of particulate matter (PM) concentration and daily mortality. Climate shifts and global planetary warming ( 3 ) could aggravate the situation. Besides, increased hospitalization (an index of morbidity) has been registered among the elderly and susceptible individuals for specific reasons. Fine and ultrafine particulate matter seems to be associated with more serious illnesses ( 6 ), as it can invade the deepest parts of the airways and more easily reach the bloodstream.

Air pollution mainly affects those living in large urban areas, where road emissions contribute the most to the degradation of air quality. There is also a danger of industrial accidents, where the spread of a toxic fog can be fatal to the populations of the surrounding areas. The dispersion of pollutants is determined by many parameters, most notably atmospheric stability and wind ( 6 ).

In developing countries ( 7 ), the problem is more serious due to overpopulation and uncontrolled urbanization along with the development of industrialization. This leads to poor air quality, especially in countries with social disparities and a lack of information on sustainable management of the environment. The use of fuels such as wood fuel or solid fuel for domestic needs due to low incomes exposes people to bad-quality, polluted air at home. It is of note that three billion people around the world are using the above sources of energy for their daily heating and cooking needs ( 8 ). In developing countries, the women of the household seem to carry the highest risk for disease development due to their longer duration exposure to the indoor air pollution ( 8 , 9 ). Due to its fast industrial development and overpopulation, China is one of the Asian countries confronting serious air pollution problems ( 10 , 11 ). The lung cancer mortality observed in China is associated with fine particles ( 12 ). As stated already, long-term exposure is associated with deleterious effects on the cardiovascular system ( 3 , 5 ). However, it is interesting to note that cardiovascular diseases have mostly been observed in developed and high-income countries rather than in the developing low-income countries exposed highly to air pollution ( 13 ). Extreme air pollution is recorded in India, where the air quality reaches hazardous levels. New Delhi is one of the more polluted cities in India. Flights in and out of New Delhi International Airport are often canceled due to the reduced visibility associated with air pollution. Pollution is occurring both in urban and rural areas in India due to the fast industrialization, urbanization, and rise in use of motorcycle transportation. Nevertheless, biomass combustion associated with heating and cooking needs and practices is a major source of household air pollution in India and in Nepal ( 14 , 15 ). There is spatial heterogeneity in India, as areas with diverse climatological conditions and population and education levels generate different indoor air qualities, with higher PM 2.5 observed in North Indian states (557–601 μg/m 3 ) compared to the Southern States (183–214 μg/m 3 ) ( 16 , 17 ). The cold climate of the North Indian areas may be the main reason for this, as longer periods at home and more heating are necessary compared to in the tropical climate of Southern India. Household air pollution in India is associated with major health effects, especially in women and young children, who stay indoors for longer periods. Chronic obstructive respiratory disease (CORD) and lung cancer are mostly observed in women, while acute lower respiratory disease is seen in young children under 5 years of age ( 18 ).

Accumulation of air pollution, especially sulfur dioxide and smoke, reaching 1,500 mg/m3, resulted in an increase in the number of deaths (4,000 deaths) in December 1952 in London and in 1963 in New York City (400 deaths) ( 19 ). An association of pollution with mortality was reported on the basis of monitoring of outdoor pollution in six US metropolitan cities ( 20 ). In every case, it seems that mortality was closely related to the levels of fine, inhalable, and sulfate particles more than with the levels of total particulate pollution, aerosol acidity, sulfur dioxide, or nitrogen dioxide ( 20 ).

Furthermore, extremely high levels of pollution are reported in Mexico City and Rio de Janeiro, followed by Milan, Ankara, Melbourne, Tokyo, and Moscow ( 19 ).

Based on the magnitude of the public health impact, it is certain that different kinds of interventions should be taken into account. Success and effectiveness in controlling air pollution, specifically at the local level, have been reported. Adequate technological means are applied considering the source and the nature of the emission as well as its impact on health and the environment. The importance of point sources and non-point sources of air pollution control is reported by Schwela and Köth-Jahr ( 21 ). Without a doubt, a detailed emission inventory must record all sources in a given area. Beyond considering the above sources and their nature, topography and meteorology should also be considered, as stated previously. Assessment of the control policies and methods is often extrapolated from the local to the regional and then to the global scale. Air pollution may be dispersed and transported from one region to another area located far away. Air pollution management means the reduction to acceptable levels or possible elimination of air pollutants whose presence in the air affects our health or the environmental ecosystem. Private and governmental entities and authorities implement actions to ensure the air quality ( 22 ). Air quality standards and guidelines were adopted for the different pollutants by the WHO and EPA as a tool for the management of air quality ( 1 , 23 ). These standards have to be compared to the emissions inventory standards by causal analysis and dispersion modeling in order to reveal the problematic areas ( 24 ). Inventories are generally based on a combination of direct measurements and emissions modeling ( 24 ).

As an example, we state here the control measures at the source through the use of catalytic converters in cars. These are devices that turn the pollutants and toxic gases produced from combustion engines into less-toxic pollutants by catalysis through redox reactions ( 25 ). In Greece, the use of private cars was restricted by tracking their license plates in order to reduce traffic congestion during rush hour ( 25 ).

Concerning industrial emissions, collectors and closed systems can keep the air pollution to the minimal standards imposed by legislation ( 26 ).

Current strategies to improve air quality require an estimation of the economic value of the benefits gained from proposed programs. These proposed programs by public authorities, and directives are issued with guidelines to be respected.

In Europe, air quality limit values AQLVs (Air Quality Limit Values) are issued for setting off planning claims ( 27 ). In the USA, the NAAQS (National Ambient Air Quality Standards) establish the national air quality limit values ( 27 ). While both standards and directives are based on different mechanisms, significant success has been achieved in the reduction of overall emissions and associated health and environmental effects ( 27 ). The European Directive identifies geographical areas of risk exposure as monitoring/assessment zones to record the emission sources and levels of air pollution ( 27 ), whereas the USA establishes global geographical air quality criteria according to the severity of their air quality problem and records all sources of the pollutants and their precursors ( 27 ).

In this vein, funds have been financing, directly or indirectly, projects related to air quality along with the technical infrastructure to maintain good air quality. These plans focus on an inventory of databases from air quality environmental planning awareness campaigns. Moreover, pollution measures of air emissions may be taken for vehicles, machines, and industries in urban areas.

Technological innovation can only be successful if it is able to meet the needs of society. In this sense, technology must reflect the decision-making practices and procedures of those involved in risk assessment and evaluation and act as a facilitator in providing information and assessments to enable decision makers to make the best decisions possible. Summarizing the aforementioned in order to design an effective air quality control strategy, several aspects must be considered: environmental factors and ambient air quality conditions, engineering factors and air pollutant characteristics, and finally, economic operating costs for technological improvement and administrative and legal costs. Considering the economic factor, competitiveness through neoliberal concepts is offering a solution to environmental problems ( 22 ).

The development of environmental governance, along with technological progress, has initiated the deployment of a dialogue. Environmental politics has created objections and points of opposition between different political parties, scientists, media, and governmental and non-governmental organizations ( 22 ). Radical environmental activism actions and movements have been created ( 22 ). The rise of the new information and communication technologies (ICTs) are many times examined as to whether and in which way they have influenced means of communication and social movements such as activism ( 28 ). Since the 1990s, the term “digital activism” has been used increasingly and in many different disciplines ( 29 ). Nowadays, multiple digital technologies can be used to produce a digital activism outcome on environmental issues. More specifically, devices with online capabilities such as computers or mobile phones are being used as a way to pursue change in political and social affairs ( 30 ).

In the present paper, we focus on the sources of environmental pollution in relation to public health and propose some solutions and interventions that may be of interest to environmental legislators and decision makers.

Sources of Exposure

It is known that the majority of environmental pollutants are emitted through large-scale human activities such as the use of industrial machinery, power-producing stations, combustion engines, and cars. Because these activities are performed at such a large scale, they are by far the major contributors to air pollution, with cars estimated to be responsible for approximately 80% of today's pollution ( 31 ). Some other human activities are also influencing our environment to a lesser extent, such as field cultivation techniques, gas stations, fuel tanks heaters, and cleaning procedures ( 32 ), as well as several natural sources, such as volcanic and soil eruptions and forest fires.

The classification of air pollutants is based mainly on the sources producing pollution. Therefore, it is worth mentioning the four main sources, following the classification system: Major sources, Area sources, Mobile sources, and Natural sources.

Major sources include the emission of pollutants from power stations, refineries, and petrochemicals, the chemical and fertilizer industries, metallurgical and other industrial plants, and, finally, municipal incineration.

Indoor area sources include domestic cleaning activities, dry cleaners, printing shops, and petrol stations.

Mobile sources include automobiles, cars, railways, airways, and other types of vehicles.

Finally, natural sources include, as stated previously, physical disasters ( 33 ) such as forest fire, volcanic erosion, dust storms, and agricultural burning.

However, many classification systems have been proposed. Another type of classification is a grouping according to the recipient of the pollution, as follows:

Air pollution is determined as the presence of pollutants in the air in large quantities for long periods. Air pollutants are dispersed particles, hydrocarbons, CO, CO 2 , NO, NO 2 , SO 3 , etc.

Water pollution is organic and inorganic charge and biological charge ( 10 ) at high levels that affect the water quality ( 34 , 35 ).

Soil pollution occurs through the release of chemicals or the disposal of wastes, such as heavy metals, hydrocarbons, and pesticides.

Air pollution can influence the quality of soil and water bodies by polluting precipitation, falling into water and soil environments ( 34 , 36 ). Notably, the chemistry of the soil can be amended due to acid precipitation by affecting plants, cultures, and water quality ( 37 ). Moreover, movement of heavy metals is favored by soil acidity, and metals are so then moving into the watery environment. It is known that heavy metals such as aluminum are noxious to wildlife and fishes. Soil quality seems to be of importance, as soils with low calcium carbonate levels are at increased jeopardy from acid rain. Over and above rain, snow and particulate matter drip into watery ' bodies ( 36 , 38 ).

Lastly, pollution is classified following type of origin:

Radioactive and nuclear pollution , releasing radioactive and nuclear pollutants into water, air, and soil during nuclear explosions and accidents, from nuclear weapons, and through handling or disposal of radioactive sewage.

Radioactive materials can contaminate surface water bodies and, being noxious to the environment, plants, animals, and humans. It is known that several radioactive substances such as radium and uranium concentrate in the bones and can cause cancers ( 38 , 39 ).

Noise pollution is produced by machines, vehicles, traffic noises, and musical installations that are harmful to our hearing.

The World Health Organization introduced the term DALYs. The DALYs for a disease or health condition is defined as the sum of the Years of Life Lost (YLL) due to premature mortality in the population and the Years Lost due to Disability (YLD) for people living with the health condition or its consequences ( 39 ). In Europe, air pollution is the main cause of disability-adjusted life years lost (DALYs), followed by noise pollution. The potential relationships of noise and air pollution with health have been studied ( 40 ). The study found that DALYs related to noise were more important than those related to air pollution, as the effects of environmental noise on cardiovascular disease were independent of air pollution ( 40 ). Environmental noise should be counted as an independent public health risk ( 40 ).

Environmental pollution occurs when changes in the physical, chemical, or biological constituents of the environment (air masses, temperature, climate, etc.) are produced.

Pollutants harm our environment either by increasing levels above normal or by introducing harmful toxic substances. Primary pollutants are directly produced from the above sources, and secondary pollutants are emitted as by-products of the primary ones. Pollutants can be biodegradable or non-biodegradable and of natural origin or anthropogenic, as stated previously. Moreover, their origin can be a unique source (point-source) or dispersed sources.

Pollutants have differences in physical and chemical properties, explaining the discrepancy in their capacity for producing toxic effects. As an example, we state here that aerosol compounds ( 41 – 43 ) have a greater toxicity than gaseous compounds due to their tiny size (solid or liquid) in the atmosphere; they have a greater penetration capacity. Gaseous compounds are eliminated more easily by our respiratory system ( 41 ). These particles are able to damage lungs and can even enter the bloodstream ( 41 ), leading to the premature deaths of millions of people yearly. Moreover, the aerosol acidity ([H+]) seems to considerably enhance the production of secondary organic aerosols (SOA), but this last aspect is not supported by other scientific teams ( 38 ).

Climate and Pollution

Air pollution and climate change are closely related. Climate is the other side of the same coin that reduces the quality of our Earth ( 44 ). Pollutants such as black carbon, methane, tropospheric ozone, and aerosols affect the amount of incoming sunlight. As a result, the temperature of the Earth is increasing, resulting in the melting of ice, icebergs, and glaciers.

In this vein, climatic changes will affect the incidence and prevalence of both residual and imported infections in Europe. Climate and weather affect the duration, timing, and intensity of outbreaks strongly and change the map of infectious diseases in the globe ( 45 ). Mosquito-transmitted parasitic or viral diseases are extremely climate-sensitive, as warming firstly shortens the pathogen incubation period and secondly shifts the geographic map of the vector. Similarly, water-warming following climate changes leads to a high incidence of waterborne infections. Recently, in Europe, eradicated diseases seem to be emerging due to the migration of population, for example, cholera, poliomyelitis, tick-borne encephalitis, and malaria ( 46 ).

The spread of epidemics is associated with natural climate disasters and storms, which seem to occur more frequently nowadays ( 47 ). Malnutrition and disequilibration of the immune system are also associated with the emerging infections affecting public health ( 48 ).

The Chikungunya virus “took the airplane” from the Indian Ocean to Europe, as outbreaks of the disease were registered in Italy ( 49 ) as well as autochthonous cases in France ( 50 ).

An increase in cryptosporidiosis in the United Kingdom and in the Czech Republic seems to have occurred following flooding ( 36 , 51 ).

As stated previously, aerosols compounds are tiny in size and considerably affect the climate. They are able to dissipate sunlight (the albedo phenomenon) by dispersing a quarter of the sun's rays back to space and have cooled the global temperature over the last 30 years ( 52 ).

Air Pollutants

The World Health Organization (WHO) reports on six major air pollutants, namely particle pollution, ground-level ozone, carbon monoxide, sulfur oxides, nitrogen oxides, and lead. Air pollution can have a disastrous effect on all components of the environment, including groundwater, soil, and air. Additionally, it poses a serious threat to living organisms. In this vein, our interest is mainly to focus on these pollutants, as they are related to more extensive and severe problems in human health and environmental impact. Acid rain, global warming, the greenhouse effect, and climate changes have an important ecological impact on air pollution ( 53 ).

Particulate Matter (PM) and Health

Studies have shown a relationship between particulate matter (PM) and adverse health effects, focusing on either short-term (acute) or long-term (chronic) PM exposure.

Particulate matter (PM) is usually formed in the atmosphere as a result of chemical reactions between the different pollutants. The penetration of particles is closely dependent on their size ( 53 ). Particulate Matter (PM) was defined as a term for particles by the United States Environmental Protection Agency ( 54 ). Particulate matter (PM) pollution includes particles with diameters of 10 micrometers (μm) or smaller, called PM 10 , and extremely fine particles with diameters that are generally 2.5 micrometers (μm) and smaller.

Particulate matter contains tiny liquid or solid droplets that can be inhaled and cause serious health effects ( 55 ). Particles <10 μm in diameter (PM 10 ) after inhalation can invade the lungs and even reach the bloodstream. Fine particles, PM 2.5 , pose a greater risk to health ( 6 , 56 ) ( Table 1 ).

Penetrability according to particle size.

Multiple epidemiological studies have been performed on the health effects of PM. A positive relation was shown between both short-term and long-term exposures of PM 2.5 and acute nasopharyngitis ( 56 ). In addition, long-term exposure to PM for years was found to be related to cardiovascular diseases and infant mortality.

Those studies depend on PM 2.5 monitors and are restricted in terms of study area or city area due to a lack of spatially resolved daily PM 2.5 concentration data and, in this way, are not representative of the entire population. Following a recent epidemiological study by the Department of Environmental Health at Harvard School of Public Health (Boston, MA) ( 57 ), it was reported that, as PM 2.5 concentrations vary spatially, an exposure error (Berkson error) seems to be produced, and the relative magnitudes of the short- and long-term effects are not yet completely elucidated. The team developed a PM 2.5 exposure model based on remote sensing data for assessing short- and long-term human exposures ( 57 ). This model permits spatial resolution in short-term effects plus the assessment of long-term effects in the whole population.

Moreover, respiratory diseases and affection of the immune system are registered as long-term chronic effects ( 58 ). It is worth noting that people with asthma, pneumonia, diabetes, and respiratory and cardiovascular diseases are especially susceptible and vulnerable to the effects of PM. PM 2.5 , followed by PM 10 , are strongly associated with diverse respiratory system diseases ( 59 ), as their size permits them to pierce interior spaces ( 60 ). The particles produce toxic effects according to their chemical and physical properties. The components of PM 10 and PM 2.5 can be organic (polycyclic aromatic hydrocarbons, dioxins, benzene, 1-3 butadiene) or inorganic (carbon, chlorides, nitrates, sulfates, metals) in nature ( 55 ).

Particulate Matter (PM) is divided into four main categories according to type and size ( 61 ) ( Table 2 ).

Types and sizes of particulate Matter (PM).

Gas contaminants include PM in aerial masses.

Particulate contaminants include contaminants such as smog, soot, tobacco smoke, oil smoke, fly ash, and cement dust.

Biological Contaminants are microorganisms (bacteria, viruses, fungi, mold, and bacterial spores), cat allergens, house dust and allergens, and pollen.

Types of Dust include suspended atmospheric dust, settling dust, and heavy dust.

Finally, another fact is that the half-lives of PM 10 and PM 2.5 particles in the atmosphere is extended due to their tiny dimensions; this permits their long-lasting suspension in the atmosphere and even their transfer and spread to distant destinations where people and the environment may be exposed to the same magnitude of pollution ( 53 ). They are able to change the nutrient balance in watery ecosystems, damage forests and crops, and acidify water bodies.

As stated, PM 2.5 , due to their tiny size, are causing more serious health effects. These aforementioned fine particles are the main cause of the “haze” formation in different metropolitan areas ( 12 , 13 , 61 ).

Ozone Impact in the Atmosphere

Ozone (O 3 ) is a gas formed from oxygen under high voltage electric discharge ( 62 ). It is a strong oxidant, 52% stronger than chlorine. It arises in the stratosphere, but it could also arise following chain reactions of photochemical smog in the troposphere ( 63 ).

Ozone can travel to distant areas from its initial source, moving with air masses ( 64 ). It is surprising that ozone levels over cities are low in contrast to the increased amounts occuring in urban areas, which could become harmful for cultures, forests, and vegetation ( 65 ) as it is reducing carbon assimilation ( 66 ). Ozone reduces growth and yield ( 47 , 48 ) and affects the plant microflora due to its antimicrobial capacity ( 67 , 68 ). In this regard, ozone acts upon other natural ecosystems, with microflora ( 69 , 70 ) and animal species changing their species composition ( 71 ). Ozone increases DNA damage in epidermal keratinocytes and leads to impaired cellular function ( 72 ).

Ground-level ozone (GLO) is generated through a chemical reaction between oxides of nitrogen and VOCs emitted from natural sources and/or following anthropogenic activities.

Ozone uptake usually occurs by inhalation. Ozone affects the upper layers of the skin and the tear ducts ( 73 ). A study of short-term exposure of mice to high levels of ozone showed malondialdehyde formation in the upper skin (epidermis) but also depletion in vitamins C and E. It is likely that ozone levels are not interfering with the skin barrier function and integrity to predispose to skin disease ( 74 ).

Due to the low water-solubility of ozone, inhaled ozone has the capacity to penetrate deeply into the lungs ( 75 ).

Toxic effects induced by ozone are registered in urban areas all over the world, causing biochemical, morphologic, functional, and immunological disorders ( 76 ).

The European project (APHEA2) focuses on the acute effects of ambient ozone concentrations on mortality ( 77 ). Daily ozone concentrations compared to the daily number of deaths were reported from different European cities for a 3-year period. During the warm period of the year, an observed increase in ozone concentration was associated with an increase in the daily number of deaths (0.33%), in the number of respiratory deaths (1.13%), and in the number of cardiovascular deaths (0.45%). No effect was observed during wintertime.

Carbon Monoxide (CO)

Carbon monoxide is produced by fossil fuel when combustion is incomplete. The symptoms of poisoning due to inhaling carbon monoxide include headache, dizziness, weakness, nausea, vomiting, and, finally, loss of consciousness.

The affinity of carbon monoxide to hemoglobin is much greater than that of oxygen. In this vein, serious poisoning may occur in people exposed to high levels of carbon monoxide for a long period of time. Due to the loss of oxygen as a result of the competitive binding of carbon monoxide, hypoxia, ischemia, and cardiovascular disease are observed.

Carbon monoxide affects the greenhouses gases that are tightly connected to global warming and climate. This should lead to an increase in soil and water temperatures, and extreme weather conditions or storms may occur ( 68 ).

However, in laboratory and field experiments, it has been seen to produce increased plant growth ( 78 ).

Nitrogen Oxide (NO 2 )

Nitrogen oxide is a traffic-related pollutant, as it is emitted from automobile motor engines ( 79 , 80 ). It is an irritant of the respiratory system as it penetrates deep in the lung, inducing respiratory diseases, coughing, wheezing, dyspnea, bronchospasm, and even pulmonary edema when inhaled at high levels. It seems that concentrations over 0.2 ppm produce these adverse effects in humans, while concentrations higher than 2.0 ppm affect T-lymphocytes, particularly the CD8+ cells and NK cells that produce our immune response ( 81 ).It is reported that long-term exposure to high levels of nitrogen dioxide can be responsible for chronic lung disease. Long-term exposure to NO 2 can impair the sense of smell ( 81 ).

However, systems other than respiratory ones can be involved, as symptoms such as eye, throat, and nose irritation have been registered ( 81 ).

High levels of nitrogen dioxide are deleterious to crops and vegetation, as they have been observed to reduce crop yield and plant growth efficiency. Moreover, NO 2 can reduce visibility and discolor fabrics ( 81 ).

Sulfur Dioxide (SO 2 )

Sulfur dioxide is a harmful gas that is emitted mainly from fossil fuel consumption or industrial activities. The annual standard for SO 2 is 0.03 ppm ( 82 ). It affects human, animal, and plant life. Susceptible people as those with lung disease, old people, and children, who present a higher risk of damage. The major health problems associated with sulfur dioxide emissions in industrialized areas are respiratory irritation, bronchitis, mucus production, and bronchospasm, as it is a sensory irritant and penetrates deep into the lung converted into bisulfite and interacting with sensory receptors, causing bronchoconstriction. Moreover, skin redness, damage to the eyes (lacrimation and corneal opacity) and mucous membranes, and worsening of pre-existing cardiovascular disease have been observed ( 81 ).

Environmental adverse effects, such as acidification of soil and acid rain, seem to be associated with sulfur dioxide emissions ( 83 ).

Lead is a heavy metal used in different industrial plants and emitted from some petrol motor engines, batteries, radiators, waste incinerators, and waste waters ( 84 ).

Moreover, major sources of lead pollution in the air are metals, ore, and piston-engine aircraft. Lead poisoning is a threat to public health due to its deleterious effects upon humans, animals, and the environment, especially in the developing countries.

Exposure to lead can occur through inhalation, ingestion, and dermal absorption. Trans- placental transport of lead was also reported, as lead passes through the placenta unencumbered ( 85 ). The younger the fetus is, the more harmful the toxic effects. Lead toxicity affects the fetal nervous system; edema or swelling of the brain is observed ( 86 ). Lead, when inhaled, accumulates in the blood, soft tissue, liver, lung, bones, and cardiovascular, nervous, and reproductive systems. Moreover, loss of concentration and memory, as well as muscle and joint pain, were observed in adults ( 85 , 86 ).

Children and newborns ( 87 ) are extremely susceptible even to minimal doses of lead, as it is a neurotoxicant and causes learning disabilities, impairment of memory, hyperactivity, and even mental retardation.

Elevated amounts of lead in the environment are harmful to plants and crop growth. Neurological effects are observed in vertebrates and animals in association with high lead levels ( 88 ).

Polycyclic Aromatic Hydrocarbons(PAHs)

The distribution of PAHs is ubiquitous in the environment, as the atmosphere is the most important means of their dispersal. They are found in coal and in tar sediments. Moreover, they are generated through incomplete combustion of organic matter as in the cases of forest fires, incineration, and engines ( 89 ). PAH compounds, such as benzopyrene, acenaphthylene, anthracene, and fluoranthene are recognized as toxic, mutagenic, and carcinogenic substances. They are an important risk factor for lung cancer ( 89 ).

Volatile Organic Compounds(VOCs)

Volatile organic compounds (VOCs), such as toluene, benzene, ethylbenzene, and xylene ( 90 ), have been found to be associated with cancer in humans ( 91 ). The use of new products and materials has actually resulted in increased concentrations of VOCs. VOCs pollute indoor air ( 90 ) and may have adverse effects on human health ( 91 ). Short-term and long-term adverse effects on human health are observed. VOCs are responsible for indoor air smells. Short-term exposure is found to cause irritation of eyes, nose, throat, and mucosal membranes, while those of long duration exposure include toxic reactions ( 92 ). Predictable assessment of the toxic effects of complex VOC mixtures is difficult to estimate, as these pollutants can have synergic, antagonistic, or indifferent effects ( 91 , 93 ).

Dioxins originate from industrial processes but also come from natural processes, such as forest fires and volcanic eruptions. They accumulate in foods such as meat and dairy products, fish and shellfish, and especially in the fatty tissue of animals ( 94 ).

Short-period exhibition to high dioxin concentrations may result in dark spots and lesions on the skin ( 94 ). Long-term exposure to dioxins can cause developmental problems, impairment of the immune, endocrine and nervous systems, reproductive infertility, and cancer ( 94 ).

Without any doubt, fossil fuel consumption is responsible for a sizeable part of air contamination. This contamination may be anthropogenic, as in agricultural and industrial processes or transportation, while contamination from natural sources is also possible. Interestingly, it is of note that the air quality standards established through the European Air Quality Directive are somewhat looser than the WHO guidelines, which are stricter ( 95 ).

Effect of Air Pollution on Health

The most common air pollutants are ground-level ozone and Particulates Matter (PM). Air pollution is distinguished into two main types:

Outdoor pollution is the ambient air pollution.

Indoor pollution is the pollution generated by household combustion of fuels.

People exposed to high concentrations of air pollutants experience disease symptoms and states of greater and lesser seriousness. These effects are grouped into short- and long-term effects affecting health.

Susceptible populations that need to be aware of health protection measures include old people, children, and people with diabetes and predisposing heart or lung disease, especially asthma.

As extensively stated previously, according to a recent epidemiological study from Harvard School of Public Health, the relative magnitudes of the short- and long-term effects have not been completely clarified ( 57 ) due to the different epidemiological methodologies and to the exposure errors. New models are proposed for assessing short- and long-term human exposure data more successfully ( 57 ). Thus, in the present section, we report the more common short- and long-term health effects but also general concerns for both types of effects, as these effects are often dependent on environmental conditions, dose, and individual susceptibility.

Short-term effects are temporary and range from simple discomfort, such as irritation of the eyes, nose, skin, throat, wheezing, coughing and chest tightness, and breathing difficulties, to more serious states, such as asthma, pneumonia, bronchitis, and lung and heart problems. Short-term exposure to air pollution can also cause headaches, nausea, and dizziness.

These problems can be aggravated by extended long-term exposure to the pollutants, which is harmful to the neurological, reproductive, and respiratory systems and causes cancer and even, rarely, deaths.

The long-term effects are chronic, lasting for years or the whole life and can even lead to death. Furthermore, the toxicity of several air pollutants may also induce a variety of cancers in the long term ( 96 ).

As stated already, respiratory disorders are closely associated with the inhalation of air pollutants. These pollutants will invade through the airways and will accumulate at the cells. Damage to target cells should be related to the pollutant component involved and its source and dose. Health effects are also closely dependent on country, area, season, and time. An extended exposure duration to the pollutant should incline to long-term health effects in relation also to the above factors.

Particulate Matter (PMs), dust, benzene, and O 3 cause serious damage to the respiratory system ( 97 ). Moreover, there is a supplementary risk in case of existing respiratory disease such as asthma ( 98 ). Long-term effects are more frequent in people with a predisposing disease state. When the trachea is contaminated by pollutants, voice alterations may be remarked after acute exposure. Chronic obstructive pulmonary disease (COPD) may be induced following air pollution, increasing morbidity and mortality ( 99 ). Long-term effects from traffic, industrial air pollution, and combustion of fuels are the major factors for COPD risk ( 99 ).

Multiple cardiovascular effects have been observed after exposure to air pollutants ( 100 ). Changes occurred in blood cells after long-term exposure may affect cardiac functionality. Coronary arteriosclerosis was reported following long-term exposure to traffic emissions ( 101 ), while short-term exposure is related to hypertension, stroke, myocardial infracts, and heart insufficiency. Ventricle hypertrophy is reported to occur in humans after long-time exposure to nitrogen oxide (NO 2 ) ( 102 , 103 ).

Neurological effects have been observed in adults and children after extended-term exposure to air pollutants.

Psychological complications, autism, retinopathy, fetal growth, and low birth weight seem to be related to long-term air pollution ( 83 ). The etiologic agent of the neurodegenerative diseases (Alzheimer's and Parkinson's) is not yet known, although it is believed that extended exposure to air pollution seems to be a factor. Specifically, pesticides and metals are cited as etiological factors, together with diet. The mechanisms in the development of neurodegenerative disease include oxidative stress, protein aggregation, inflammation, and mitochondrial impairment in neurons ( 104 ) ( Figure 1 ).

Impact of air pollutants on the brain.

Brain inflammation was observed in dogs living in a highly polluted area in Mexico for a long period ( 105 ). In human adults, markers of systemic inflammation (IL-6 and fibrinogen) were found to be increased as an immediate response to PNC on the IL-6 level, possibly leading to the production of acute-phase proteins ( 106 ). The progression of atherosclerosis and oxidative stress seem to be the mechanisms involved in the neurological disturbances caused by long-term air pollution. Inflammation comes secondary to the oxidative stress and seems to be involved in the impairment of developmental maturation, affecting multiple organs ( 105 , 107 ). Similarly, other factors seem to be involved in the developmental maturation, which define the vulnerability to long-term air pollution. These include birthweight, maternal smoking, genetic background and socioeconomic environment, as well as education level.

However, diet, starting from breast-feeding, is another determinant factor. Diet is the main source of antioxidants, which play a key role in our protection against air pollutants ( 108 ). Antioxidants are free radical scavengers and limit the interaction of free radicals in the brain ( 108 ). Similarly, genetic background may result in a differential susceptibility toward the oxidative stress pathway ( 60 ). For example, antioxidant supplementation with vitamins C and E appears to modulate the effect of ozone in asthmatic children homozygous for the GSTM1 null allele ( 61 ). Inflammatory cytokines released in the periphery (e.g., respiratory epithelia) upregulate the innate immune Toll-like receptor 2. Such activation and the subsequent events leading to neurodegeneration have recently been observed in lung lavage in mice exposed to ambient Los Angeles (CA, USA) particulate matter ( 61 ). In children, neurodevelopmental morbidities were observed after lead exposure. These children developed aggressive and delinquent behavior, reduced intelligence, learning difficulties, and hyperactivity ( 109 ). No level of lead exposure seems to be “safe,” and the scientific community has asked the Centers for Disease Control and Prevention (CDC) to reduce the current screening guideline of 10 μg/dl ( 109 ).

It is important to state that impact on the immune system, causing dysfunction and neuroinflammation ( 104 ), is related to poor air quality. Yet, increases in serum levels of immunoglobulins (IgA, IgM) and the complement component C3 are observed ( 106 ). Another issue is that antigen presentation is affected by air pollutants, as there is an upregulation of costimulatory molecules such as CD80 and CD86 on macrophages ( 110 ).

As is known, skin is our shield against ultraviolet radiation (UVR) and other pollutants, as it is the most exterior layer of our body. Traffic-related pollutants, such as PAHs, VOCs, oxides, and PM, may cause pigmented spots on our skin ( 111 ). On the one hand, as already stated, when pollutants penetrate through the skin or are inhaled, damage to the organs is observed, as some of these pollutants are mutagenic and carcinogenic, and, specifically, they affect the liver and lung. On the other hand, air pollutants (and those in the troposphere) reduce the adverse effects of ultraviolet radiation UVR in polluted urban areas ( 111 ). Air pollutants absorbed by the human skin may contribute to skin aging, psoriasis, acne, urticaria, eczema, and atopic dermatitis ( 111 ), usually caused by exposure to oxides and photochemical smoke ( 111 ). Exposure to PM and cigarette smoking act as skin-aging agents, causing spots, dyschromia, and wrinkles. Lastly, pollutants have been associated with skin cancer ( 111 ).

Higher morbidity is reported to fetuses and children when exposed to the above dangers. Impairment in fetal growth, low birth weight, and autism have been reported ( 112 ).

Another exterior organ that may be affected is the eye. Contamination usually comes from suspended pollutants and may result in asymptomatic eye outcomes, irritation ( 112 ), retinopathy, or dry eye syndrome ( 113 , 114 ).

Environmental Impact of Air Pollution

Air pollution is harming not only human health but also the environment ( 115 ) in which we live. The most important environmental effects are as follows.

Acid rain is wet (rain, fog, snow) or dry (particulates and gas) precipitation containing toxic amounts of nitric and sulfuric acids. They are able to acidify the water and soil environments, damage trees and plantations, and even damage buildings and outdoor sculptures, constructions, and statues.

Haze is produced when fine particles are dispersed in the air and reduce the transparency of the atmosphere. It is caused by gas emissions in the air coming from industrial facilities, power plants, automobiles, and trucks.

Ozone , as discussed previously, occurs both at ground level and in the upper level (stratosphere) of the Earth's atmosphere. Stratospheric ozone is protecting us from the Sun's harmful ultraviolet (UV) rays. In contrast, ground-level ozone is harmful to human health and is a pollutant. Unfortunately, stratospheric ozone is gradually damaged by ozone-depleting substances (i.e., chemicals, pesticides, and aerosols). If this protecting stratospheric ozone layer is thinned, then UV radiation can reach our Earth, with harmful effects for human life (skin cancer) ( 116 ) and crops ( 117 ). In plants, ozone penetrates through the stomata, inducing them to close, which blocks CO 2 transfer and induces a reduction in photosynthesis ( 118 ).

Global climate change is an important issue that concerns mankind. As is known, the “greenhouse effect” keeps the Earth's temperature stable. Unhappily, anthropogenic activities have destroyed this protecting temperature effect by producing large amounts of greenhouse gases, and global warming is mounting, with harmful effects on human health, animals, forests, wildlife, agriculture, and the water environment. A report states that global warming is adding to the health risks of poor people ( 119 ).

People living in poorly constructed buildings in warm-climate countries are at high risk for heat-related health problems as temperatures mount ( 119 ).

Wildlife is burdened by toxic pollutants coming from the air, soil, or the water ecosystem and, in this way, animals can develop health problems when exposed to high levels of pollutants. Reproductive failure and birth effects have been reported.

Eutrophication is occurring when elevated concentrations of nutrients (especially nitrogen) stimulate the blooming of aquatic algae, which can cause a disequilibration in the diversity of fish and their deaths.

Without a doubt, there is a critical concentration of pollution that an ecosystem can tolerate without being destroyed, which is associated with the ecosystem's capacity to neutralize acidity. The Canada Acid Rain Program established this load at 20 kg/ha/yr ( 120 ).

Hence, air pollution has deleterious effects on both soil and water ( 121 ). Concerning PM as an air pollutant, its impact on crop yield and food productivity has been reported. Its impact on watery bodies is associated with the survival of living organisms and fishes and their productivity potential ( 121 ).

An impairment in photosynthetic rhythm and metabolism is observed in plants exposed to the effects of ozone ( 121 ).

Sulfur and nitrogen oxides are involved in the formation of acid rain and are harmful to plants and marine organisms.

Last but not least, as mentioned above, the toxicity associated with lead and other metals is the main threat to our ecosystems (air, water, and soil) and living creatures ( 121 ).

In 2018, during the first WHO Global Conference on Air Pollution and Health, the WHO's General Director, Dr. Tedros Adhanom Ghebreyesus, called air pollution a “silent public health emergency” and “the new tobacco” ( 122 ).

Undoubtedly, children are particularly vulnerable to air pollution, especially during their development. Air pollution has adverse effects on our lives in many different respects.

Diseases associated with air pollution have not only an important economic impact but also a societal impact due to absences from productive work and school.

Despite the difficulty of eradicating the problem of anthropogenic environmental pollution, a successful solution could be envisaged as a tight collaboration of authorities, bodies, and doctors to regularize the situation. Governments should spread sufficient information and educate people and should involve professionals in these issues so as to control the emergence of the problem successfully.

Technologies to reduce air pollution at the source must be established and should be used in all industries and power plants. The Kyoto Protocol of 1997 set as a major target the reduction of GHG emissions to below 5% by 2012 ( 123 ). This was followed by the Copenhagen summit, 2009 ( 124 ), and then the Durban summit of 2011 ( 125 ), where it was decided to keep to the same line of action. The Kyoto protocol and the subsequent ones were ratified by many countries. Among the pioneers who adopted this important protocol for the world's environmental and climate “health” was China ( 3 ). As is known, China is a fast-developing economy and its GDP (Gross Domestic Product) is expected to be very high by 2050, which is defined as the year of dissolution of the protocol for the decrease in gas emissions.

A more recent international agreement of crucial importance for climate change is the Paris Agreement of 2015, issued by the UNFCCC (United Nations Climate Change Committee). This latest agreement was ratified by a plethora of UN (United Nations) countries as well as the countries of the European Union ( 126 ). In this vein, parties should promote actions and measures to enhance numerous aspects around the subject. Boosting education, training, public awareness, and public participation are some of the relevant actions for maximizing the opportunities to achieve the targets and goals on the crucial matter of climate change and environmental pollution ( 126 ). Without any doubt, technological improvements makes our world easier and it seems difficult to reduce the harmful impact caused by gas emissions, we could limit its use by seeking reliable approaches.

Synopsizing, a global prevention policy should be designed in order to combat anthropogenic air pollution as a complement to the correct handling of the adverse health effects associated with air pollution. Sustainable development practices should be applied, together with information coming from research in order to handle the problem effectively.

At this point, international cooperation in terms of research, development, administration policy, monitoring, and politics is vital for effective pollution control. Legislation concerning air pollution must be aligned and updated, and policy makers should propose the design of a powerful tool of environmental and health protection. As a result, the main proposal of this essay is that we should focus on fostering local structures to promote experience and practice and extrapolate these to the international level through developing effective policies for sustainable management of ecosystems.

Author Contributions

All authors listed have made a substantial, direct and intellectual contribution to the work, and approved it for publication.

Conflict of Interest

IM is employed by the company Delphis S.A. The remaining authors declare that the present review paper was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Industrial Air Pollution: A case study on Bawana Industrial Area

Industrial emissions are a major source of respirable particulate matter, especially in urban and metropolitan areas. The main pollutants associated with industrial pollution are toxic heavy metals, volatile organic carbon (VOC’s), polyaromatic hydrocarbons (PAH’s), PM10 and PM2.5 which can have serious repercussions on not just human health but also on the environment as a whole. Currently, there are several approaches to consider these missions.However, the uncertainty of the quantification of these emissions is very high. Hence it is necessary to assess the quality of the existing emission factors in order to improve them as well as to verify them. Moreover, it is a well-known fact that the impacts and effects of industrial pollution have been more pronounced in cities of developing countries due to lack of significant advancement in technologies pertaining to air pollution. This work provides an in-depth analysis of the composition of the various aforementioned pollutants involved in industrial air pollution. It also urges the environmental authorities to closely monitor these hazardous sources of pollution as well as consider the possibility of narrowing the emission standard limits set for industries, and at the same time encourage the scientific community to improve existing methods to estimate and validate these emissions.

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Four IUCN economic case studies show the impacts of plastic pollution in the marine environment on biodiversity, livelihoods, and more in Africa and Asia

Research into the economic aspects of the Marine Plastics and Coastal Communities project, to contain and reduce plastic pollution in the ocean, delivers insight into the true costs of plastic pollution on communities, livelihoods, coasts, and the global ocean.

Photo: Adobe Stock Image

The objective

The Marine Plastics and Coastal Communities (MARPLASTICCs) project goal was to assist governments and regional bodies in Eastern and Southern Africa and Asia to promote, enact, and enforce legislation and other effective measures to contain and reduce plastic pollution in the ocean. Part of the research completed included defining an economic assessment approach and producing economics case studies that reflected the impacts of plastic pollution on the marine environment, on coastal livelihoods, and more.

National case studies

Four national level economic case studies are available: for Mozambique, South Africa, Thailand, and Viet Nam. The important economic sectors of fisheries and tourism were studied, using different lenses to examine how plastic pollution causes detrimental economic impacts at national and local levels. Each assessment differs and explores wide-ranging economic dimensions that should be considered when creating a national plan of action to mitigate marine litter and plastic pollution in the environment. From impacts upon export revenue, employment and food security, to the economic efficiency of beach cleaning in conjunction with deposit refund schemes, and the impact of ghost gear on fisheries, these four case studies take a reader into the true costs of plastic pollution on our global ocean and coastal communities.

Mozambique Economic Report

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IUCN works on-the-ground with partners from NGOs, the private sector, and national governments, in order to determine the priority problems and the most effective interventions, to advise countries how to stop the problem within their specific national context. IUCN bring science and knowledge together with policy, for action, in this case economic policies can be examined for their role in dealing with plastic pollution.

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Acknowledgments and Support

The Marine Plastics and Coastal Communities project (MARPLASTICCs), generously supported by the Swedish International Development Cooperation Agency (Sida), provided  support for the research and production of these Economic Case Studies.

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Natural Disaster, Tax Avoidance, and Corporate Pollution Emissions: Evidence from China

• Original Paper
• Published: 23 May 2024

Cite this article

• Rui Xu 1 , 2 &
• Liuyang Ren 1  

Our study explores how climate risk affects the tax behavior of governments and local firms, subsequently affecting corporate pollution emissions. Using data on Chinese non-state-owned industrial enterprises from 1998 to 2014, we empirically investigate the impact of natural disasters on corporate tax avoidance. The results indicate that companies in earthquake-damaged areas are less likely to avoid taxes than those in unaffected areas. Furthermore, companies that pay more taxes after a disaster can secure favorable government environmental policies, as indicated by a rise in pollution emissions. Moreover, this effect is more pronounced for less polluting firms and firms with higher financial constraints. Our study contributes to the literature on taxation and ESG from the perspective of favor-exchange in government–firm relationships.

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Data availability

The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.

The risk appears to be manifesting itself along several physical dimensions: a) earthquake risk, which can cause extensive damages in a relatively short period; b) hurricane risk, which has increased in intensity and frequency in different parts of the world; c) drought risk, occur in some particular regions; d) flood risk, affecting predominantly some regions; e) heat risk, which refers to increase in average temperatures over time.

Tax-sharing system gives Chinese local governments tax autonomy to control local corporate taxes.

See the Chinese National Earthquake Response Plan on this page https://www.gov.cn/yjgl/2012-09/21/content_ 2,230,337.htm. (Notice this page is in Chinese; Google Translate can be used to view the content.).

See Earthquake Response Plan in Huangshan City on this page https://www.huangshan.gov.cn/zwgk/public /6615714/10703207.htm. (Notice this page is in Chinese; Google Translate can be used to view the content.).

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Acknowledgements

This work was supported by the National Natural Science Foundation Project of China (Grant No.72302061), the Guangdong Office of Philosophy and Social Science (Project GD23YGL21) and Philosophy and Social Science Foundation of Guangzhou (Project 2023GZGJ58). The corresponding author is Liuyang Ren. All errors remain ours. All co-authors make equal contributions to the formation of this paper.

Guangdong Office of Philosophy and Social Science, GD23YGL21, Liuyang Ren, National Natural Science Foundation of China, 72302061, Liuyang Ren, Philosophy and Social Science Foundation of Guangzhou, 2023GZGJ58, Rui Xu.

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Xu, R., Ren, L. Natural Disaster, Tax Avoidance, and Corporate Pollution Emissions: Evidence from China. J Bus Ethics (2024). https://doi.org/10.1007/s10551-024-05716-w

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Received : 24 August 2023

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Published : 23 May 2024

DOI : https://doi.org/10.1007/s10551-024-05716-w

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