Air Pollution: Who's At Risk And Why?

Air pollution is a pressing global health concern, with almost the entire global population (99%) breathing air that exceeds the recommended guideline limits. While air pollution is unhealthy for everyone, certain groups are more vulnerable than others. These groups include children, pregnant women, older adults, and individuals with pre-existing heart and lung disease. Socioeconomic factors also play a role, with low-income communities, rural areas, and people of color bearing the brunt of air pollution exposure. Additionally, proximity to industrial sources of pollution, underlying health issues, poor nutrition, and stress can further increase susceptibility to the harmful effects of air pollution. Understanding these risk factors is crucial for developing strategies to protect vulnerable populations and mitigate the adverse health impacts of air pollution.

Pre-existing disease

People with pre-existing health conditions are more vulnerable to the adverse effects of air pollution. The elderly, children, and pregnant women are also more susceptible to air pollution-related diseases. Genetics, comorbidities, nutrition, and sociodemographic factors all play a role in an individual's susceptibility to air pollution.

Air pollution is the presence of harmful substances in the atmosphere, such as dust, fumes, gases, and smoke, which can have detrimental effects on human health. It is the leading environmental health risk in Europe and a significant cause of premature death and disease worldwide. Fine particulate matter (PM2.5) is the air pollutant that causes the most harm and premature mortality.

People with pre-existing respiratory disorders are particularly vulnerable to the effects of air pollution. Climate change and meteorological factors, such as heatwaves, can amplify air pollution levels, leading to increased respiratory issues and hospitalizations. Studies have shown that higher exposure to PM2.5 results in higher numbers of premature deaths and disabilities related to respiratory diseases, such as chronic obstructive pulmonary disease.

In addition to respiratory diseases, air pollution is linked to a range of other health issues. These include stroke, ischaemic heart disease, lung cancer, pneumonia, and cataract (from household air pollution). There is also evidence of a link between air pollution and an increased risk of adverse pregnancy outcomes, diabetes, cognitive impairment, neurological diseases, obesity, systemic inflammation, Alzheimer's disease, and dementia.

The impact of air pollution on health can vary across different populations and geographical locations. Socio-economic status is a factor, with lower-income communities often facing higher exposure to air pollution due to their proximity to busy roads or industrial areas. Additionally, certain genetic, nutritional, and sociodemographic factors can influence an individual's susceptibility to the health effects of air pollution.

Genetic profile

It is increasingly clear that genetic background is an important factor in determining susceptibility to air pollutants. Genetic predispositions, combined with internal and external factors, contribute to individual responses to air pollutants.

Internal factors include sex, age, diet, and predisposing diseases (e.g. asthma, diabetes, chronic obstructive pulmonary disease, and increased body mass index). External factors include physical forces (e.g. temperature, altitude), socioeconomic status, and previous exposure.

Genetic linkage studies have been used to identify chromosomal regions linked to the effects of air pollutants, particularly ozone (O3) and particulates. For example, linkage analyses using inbred mice identified chromosomal segments (quantitative trait loci, or QTLs) with genes controlling susceptibility to lung inflammation (chromosome 17), injury (chromosome 11), and hyperpermeability (chromosome 4) in response to ozone exposure. Similar genetic mechanisms may control pulmonary responses to sulphate-associated particles, as the same chromosome 17 and 11 QTLs are linked to immune dysfunction induced by these particles. Candidate genes within the QTLs on chromosomes 4 and 17 include the toll-like receptor 4 and the pro-inflammatory cytokine, tumour necrosis factor-alpha, respectively.

Polymorphisms in oxidative stress genes (GSTM1, GSTP1) have been shown to alter the response to combined exposure to ragweed pollen and diesel exhaust particles. In Mexico City, which has chronically high ozone levels, polymorphisms in the GSTM1 gene have been used to predict which asthma patients would benefit from antioxidant supplementation.

While genetic factors play a role in susceptibility to air pollutants, it is important to note that the interaction between age and genetic background in the development of air pollution-induced diseases requires further study.

Age

Children are at an increased risk due to their developing respiratory and immune systems, which may be more susceptible to the harmful impacts of pollutants. Additionally, they tend to breathe faster and take in more air relative to their body weight, potentially increasing their exposure to harmful substances. Evidence suggests that air pollution can contribute to respiratory infections, aggravated asthma, and reduced lung function in children. Prolonged exposure may also impact their neurological development and increase the risk of other health issues, such as diabetes.

For the elderly, the risks are also heightened due to age-related physiological changes and potential underlying health conditions. Older individuals may have weaker immune systems and reduced lung capacity, making them more susceptible to the harmful effects of air pollutants. They are at an increased risk of developing cardiovascular and respiratory diseases, such as ischaemic heart disease, chronic obstructive pulmonary disease, and pneumonia.

The vulnerability of these age groups is further exacerbated by their potential dependence on others for care. Children and the elderly may not have complete autonomy over their exposure to air pollutants and may require assistance in taking protective measures. Additionally, they may be more likely to reside in areas with higher pollution levels, such as near busy roads or industrial zones, due to economic or logistical factors.

Furthermore, age interacts with other factors, such as genetics and pre-existing health conditions, to influence susceptibility. For example, older individuals with cardiovascular or respiratory diseases are at a heightened risk of adverse health outcomes from air pollution. Similarly, genetic predispositions may be triggered or exacerbated by exposure to pollutants, and age can influence the expression of these genetic factors.

While age is a critical aspect, it is important to recognize that the interplay of various factors, including genetics, comorbidities, nutrition, and sociodemographic influences, contributes to an individual's overall susceptibility to air pollutants. The complex interaction of these factors across different age groups continues to be an area of ongoing research.

Sex

Several factors and characteristics may account for heightened susceptibility to air pollution. Sex is one of these factors, with studies indicating potential increased risks of PM-related health effects by sex and race/ethnicity. However, these associations are not always consistent across health effects, PM size fractions, or study locations.

The effects of air pollution on health can vary between men and women due to biological sex differences and gendered exposures. For instance, in a 13-year follow-up of Krakow adults, residence in higher sulfate areas better predicted FEV1 decrements among men than among women. Among women, SO2 and PM correlated with symptoms, possibly due to women spending more time near home.

Gender analysis aims to disentangle social from biological differences between males and females, which may help explain the potential sources of effect modification. For example, gender affects the presence of exposure (e.g., cosmetic use), while biological sex differences determine the consequent dose (e.g., through dermal thickness and permeability).

Additionally, researchers may differentiate sex-linked biological effects, such as target organs and hormonal composition, which can differ significantly between men and women. These biological differences may increase susceptibility to specific illnesses directly involving biological parameters, such as sex organs and hormonal composition.

Furthermore, examining exposure and disease patterns across societies with varying measures of gender equity may offer insights into the root causes of susceptibility differences. However, disentangling gender and sex effects in air pollution-health associations among children may be more complicated due to differing lung function growth rates between sexes.

Race and ethnicity

Several studies have found that racial and ethnic minorities are exposed to higher levels of air pollution and are more susceptible to the harmful effects of air pollutants. Research has shown that non-white populations, especially Black people, face a higher risk from particle pollution. This is true even when controlling for income level, suggesting that race and ethnicity are independent drivers of these disparities.

A 2016 study of New Jersey residents found that the risk of premature death from long-term exposure to particle pollution was higher in communities with larger African American populations. Similarly, studies of Atlanta, GA, found that particle pollution increased the risk of asthma attacks in zip codes with higher poverty rates and among people eligible for Medicaid. These findings indicate that socioeconomic factors, such as poverty and access to healthcare, may also contribute to the increased vulnerability of racial and ethnic minority groups.

Hispanic and Asian populations have also been found to have a higher risk of premature death from particle pollution than whites. This risk is not solely due to income disparities, as higher-income individuals from these racial groups still face greater health risks than lower-income whites. Chronic stress as a result of discrimination and residential segregation, which have led to higher exposure to air pollution in predominantly non-white communities, are believed to be contributing factors.

Furthermore, a 2021 study published in Science Advances found that PM2.5 polluters disproportionately affect people of color in the United States. The study analyzed EPA data from over 5,000 emission source types and found racial and ethnic disparities in exposure levels for almost all major emission categories. White people were exposed to lower than average concentrations from emission sources, while people of color experienced greater than average exposures from the same sources. These disparities were consistent across states, urban and rural areas, and income levels.

The American Lung Association and Harvard T.H. Chan School of Public Health have also highlighted the stark disparities in air pollution exposure among racial and ethnic minorities and low-income groups in the United States. Their research emphasizes the need for targeted air pollution reduction strategies to protect these vulnerable populations from environmental hazards.

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