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Traffic and power generation are the main sources of urban air pollution. The idea that outdoor air pollution can cause exacerbations of pre-existing asthma is supported by an evidence base that has been accumulating for several decades, with several studies suggesting a contribution to new-onset asthma as well. In this Series paper, we discuss the effects of particulate matter (PM), gaseous pollutants (ozone, nitrogen dioxide, and sulphur dioxide), and mixed traffic-related air pollution. We focus on clinical studies, both epidemiological and experimental, published in the previous 5 years. From a mechanistic perspective, air pollutants probably cause oxidative injury to the airways, leading to inflammation, remodelling, and increased risk of sensitisation. Although several pollutants have been linked to new-onset asthma, the strength of the evidence is variable. We also discuss clinical implications, policy issues, and research gaps relevant to air pollution and asthma.

When catastrophic wildfires come near populated urban areas, as recently occurred in California, many people are exposed to relatively high levels of smoke. How should physicians advise patients and the public when they’re facing poor air quality due to wildfire smoke?

Workplace inhalational hazards remain common worldwide, even though they are ameliorable. Previous American Thoracic Society documents have assessed the contribution of workplace exposures to asthma and chronic obstructive pulmonary disease on a population level, but not to other chronic respiratory diseases. The goal of this document is to report an in-depth literature review and data synthesis of the occupational contribution to the burden of the major nonmalignant respiratory diseases, including airway diseases; interstitial fibrosis; hypersensitivity pneumonitis; other noninfectious granulomatous lung diseases, including sarcoidosis; and selected respiratory infections. Relevant literature was identified for each respiratory condition. The occupational population attributable fraction (PAF) was estimated for those conditions for which there were sufficient population-based studies to allow pooled estimates. For the other conditions, the occupational burden of disease was estimated on the basis of attribution in case series, incidence rate ratios, or attributable fraction within an exposed group. Workplace exposures contribute substantially to the burden of multiple chronic respiratory diseases, including asthma (PAF, 16%); chronic obstructive pulmonary disease (PAF, 14%); chronic bronchitis (PAF, 13%); idiopathic pulmonary fibrosis (PAF, 26%); hypersensitivity pneumonitis (occupational burden, 19%); other granulomatous diseases, including sarcoidosis (occupational burden, 30%); pulmonary alveolar proteinosis (occupational burden, 29%); tuberculosis (occupational burden, 2.3% in silica-exposed workers and 1% in healthcare workers); and community-acquired pneumonia in working-age adults (PAF, 10%). Workplace exposures contribute to the burden of disease across a range of nonmalignant lung conditions in adults (in addition to the 100% burden for the classic occupational pneumoconioses). This burden has important clinical, research, and policy implications. There is a pressing need to improve clinical recognition and public health awareness of the contribution of occupational factors across a range of nonmalignant respiratory diseases.

Wildfire activity is predicted to increase in many parts of the world due to changes in temperature and precipitation patterns from global climate change. Wildfire smoke contains numerous hazardous air pollutants and many studies have documented population health effects from this exposure. We aimed to assess the evidence of health effects from exposure to wildfire smoke and to identify susceptible populations. We reviewed the scientific literature for studies of wildfire smoke exposure on mortality and on respiratory, cardiovascular, mental, and perinatal health. Within those reviewed papers deemed to have minimal risk of bias, we assessed the coherence and consistency of findings. Consistent evidence documents associations between wildfire smoke exposure and general respiratory health effects, specifically exacerbations of asthma and chronic obstructive pulmonary disease. Growing evidence suggests associations with increased risk of respiratory infections and all-cause mortality. Evidence for cardiovascular effects is mixed, but a few recent studies have reported associations for specific cardiovascular end points. Insufficient research exists to identify specific population subgroups that are more susceptible to wildfire smoke exposure. Consistent evidence from a large number of studies indicates that wildfire smoke exposure is associated with respiratory morbidity with growing evidence supporting an association with all-cause mortality. More research is needed to clarify which causes of mortality may be associated with wildfire smoke, whether cardiovascular outcomes are associated with wildfire smoke, and if certain populations are more susceptible. Reid CE, Brauer M, Johnston FH, Jerrett M, Balmes JR, Elliott CT. 2016. Critical review of health impacts of wildfire smoke exposure. Environ Health Perspect 124:1334-1343; http://dx.doi.org/10.1289/ehp.1409277.

Wildfire smoke is an increasing environmental health threat to which children are particularly vulnerable, for both physiologic and behavioral reasons. To address the need for improved public health messaging this review summarizes current knowledge and knowledge gaps in the health effects of wildfire smoke in children, as well as tools for public health response aimed at children, including consideration of low-cost sensor data, respirators, and exposures in school environments. There is an established literature of health effects in children from components of ambient air pollution, which are also present in wildfire smoke, and an emerging literature on the effects of wildfire smoke, particularly for respiratory outcomes. Low-cost particulate sensors demonstrate the spatial variability of pollution, including wildfire smoke, where children live and play. Surgical masks and respirators can provide limited protection for children during wildfire events, with expected decreases of roughly 20% and 80% for surgical masks and N95 respirators, respectively. Schools should improve filtration to reduce exposure of our nation’s children to smoke during wildfire events. The evidence base described may help clinical and public health authorities provide accurate information to families to improve their decision making.

The link between particulate pollution and mortality was originally recognized in the context of severe episodes of poor air quality in the 20th century, such as the London Fog of 1952. 1 These episodes showed clear evidence that the number of deaths increased in association with high levels of particulate matter (PM). The policy response to the increasing evidence of the effects of air pollution on public health was for governments to develop air-quality regulations. In the United States, the Clean Air Act of 1970 mandated that the Environmental Protection Agency (EPA) develop national ambient air-quality standards (NAAQS) to protect even . . .

Though SARS-CoV-2 outbreaks have been documented in occupational settings and in-person essential work has been suspected as a risk factor for COVID-19, occupational differences in excess mortality have, to date, not been examined. Such information could point to opportunities for intervention, such as vaccine prioritization or regulations to enforce safer work environments. Using autoregressive integrated moving average models and California Department of Public Health data representing 356,188 decedents 18-65 years of age who died between January 1, 2016 and November 30, 2020, we estimated pandemic-related excess mortality by occupational sector and occupation, with additional stratification of the sector analysis by race/ethnicity. During these first 9 months of the COVID-19 pandemic, working-age adults experienced 11,628 more deaths than expected, corresponding to 22% relative excess and 46 excess deaths per 100,000 living individuals. Sectors with the highest relative and per-capita excess mortality were food/agriculture (39% relative excess; 75 excess deaths per 100,000), transportation/logistics (31%; 91 per 100,000), manufacturing (24%; 61 per 100,000), and facilities (23%; 83 per 100,000). Across racial and ethnic groups, Latino working-age Californians experienced the highest relative excess mortality (37%) with the highest excess mortality among Latino workers in food and agriculture (59%; 97 per 100,000). Black working-age Californians had the highest per-capita excess mortality (110 per 100,000), with relative excess mortality highest among transportation/logistics workers (36%). Asian working-age Californians had lower excess mortality overall, but notable relative excess mortality among health/emergency workers (37%), while White Californians had high per-capita excess deaths among facilities workers (70 per 100,000). Certain occupational sectors are associated with high excess mortality during the pandemic, particularly among racial and ethnic groups also disproportionately affected by COVID-19. In-person essential work is a likely venue of transmission of coronavirus infection and must be addressed through vaccination and strict enforcement of health orders in workplace settings.

Ambient air pollutants such as particulate matter (PM), ozone (O3), and nitrogen dioxide (NO2) have been associated with lower lung function among children. However, the reported associations could be due to correlation with other pollutants. We investigate the relationships between exposures to eight ambient air pollutants and children's lung function and apply mixture analysis to identify key contributors to health effects. The Children's Health and Air Pollution Study (CHAPS) in Fresno, California, is a prospective cohort study that recruited 299 children and assessed their lung function at two visits, at approximately 7 and 9 years of age. The children's forced expiratory volume in the first second (FEV1), forced vital capacity (FVC), and FEV1/FVC ratio were standardized using the Global Lung Function Initiative (GLI) race-neutral calculators. We assessed the children's average daily residential exposures to PM2.5, PM10, nitrogen oxides (NOx), NO2, O3, carbon monoxide (CO), elemental carbon (EC), and polycyclic aromatic hydrocarbons (PAHs), during the 1-week, 1-month, 3-month, 6-month, and 12-month periods before each visit, and the 2 years between visits. We applied linear mixed-effect models and quantile-based g-computation (q-gcomp) for statistical analysis. The children's exposures to the eight ambient air pollutants exhibited high intercorrelation: Seven air pollutants were positively correlated, while O3 exposures were negatively correlated with the other pollutants. Higher PM10 was associated with lower FEV1 and FEV1/FVC ratio, and the associations were strongest for the 3-month exposure timeframe. Q-gcomp also identified PM10 as the key pollutant associated with lower FEV1 and FEV1/FVC ratio. Among the eight ambient air pollutants, PM10 was the strongest risk factor for impaired lung function among children in Fresno. Ambient air pollution levels in this community exceed regulatory standards and are harmful to children's lung function.

Hypertension is a leading risk factor for cardiovascular disease, and its association with household air pollution (HAP) in sub-Saharan Africa is understudied. To investigate the association between blood pressure (BP) and HAP exposure in a population-based cohort in rural Malawi. In the Chikwawa district, the site of a previous randomized controlled trial of a cleaner-burning cookstove intervention (the Cooking and Pneumonia Study or CAPS), we recruited 1,481 randomly selected adults. A subset (∼21%) were from participating households in CAPS. This cross-sectional analysis investigates associations of BP with stove type and, in a sample of participants, with particulate matter ≤ 2.5 μm diameter (PM2.5) and carbon monoxide (CO), both measured using 48-hour personal monitoring. Two main types of analysis were conducted: a) assessment of differences in mean systolic BP (SPB) and diastolic BP (DBP) among three groups based on stove use/type and b) assessment of the associations between PM2.5 and CO with mean SBP and DBP; both analyses using multivariable linear regression. Of the 1481 participants, 910 provided BP data. There was no difference for either mean SBP or DBP between the CAPS intervention and control groups. However, when comparing all CAPS participants (i.e., those provided cleaner-burning cookstoves by study's end) to the non-CAPS group, mean SBP was reduced (-3.53 mmHg, 95% CI:-6.54,-0.52), but not DBP (-0.73 mmHg, 95% CI:-2.36,0.90). Of these, 599 participants also had ≥24 hours personal exposure monitoring data. Neither the log mean PM2.5 concentration nor the log mean CO concentration was associated with either SBP or DBP. In this cross-sectional study in non-pregnant adults to measure both exposure to HAP and blood pressure in sub-Saharan Africa, we found evidence for an association between receiving a cleaner-burning cookstove and reduced SBP, but no evidence for an association between BP and personal exposure to PM2.5 or CO.