We assessed the health risks of fine particulate matter (PM_2.5) ambient air pollution and its trace elemental components in a rural South African community. Air pollution is the largest environmental cause of disease and disproportionately affects low- and middle-income countries. PM_2.5 samples were previously collected, April 2017 to April 2018, and PM_2.5 mass determined. The filters were analyzed for chemical composition. The United States Environmental Protection Agency’s (US EPA) health risk assessment method was applied. Reference doses were calculated from the World Health Organization (WHO) guidelines, South African National Ambient Air Quality Standards (NAAQS), and US EPA reference concentrations. Despite relatively moderate levels of PM_2.5 the health risks were substantial, especially for infants and children. The average annual PM_2.5 concentration was 11 µg/m³, which is above WHO guidelines, but below South African NAAQS. Adults were exposed to health risks from PM_2.5 during May to October, whereas infants and children were exposed to risk throughout the year. Particle-bound nickel posed both non-cancer and cancer risks. We conclude that PM_2.5 poses health risks in Thohoyandou, despite levels being compliant with yearly South African NAAQS. The results indicate that air quality standards need to be tightened and PM_2.5 levels lowered in South Africa.

Background: Despite accumulating evidence of an association between air pollution and renal disease, studies on the association between long-term exposure to air pollution and renal function are still contradictory. This study aimed to investigate this association in a large population with relatively low exposure and with improved estimation of renal function as well as renal injury biomarkers. Methods: We performed a cross-sectional analysis in the middle-aged general population participating in the Swedish CardioPulmonary bioImaging Study (SCAPIS; n = 30 154). Individual 10-year exposure to total and locally emitted fine particulate matter (PM_2.5), inhalable particulate matter (PM₁₀), and nitrogen oxides (NO_x) were modelled using high-resolution dispersion models. Linear regression models were used to estimate associations between exposures and estimated glomerular filtration rate (eGFR, combined creatinine and cystatin C) and serum levels of renal injury biomarkers (KIM-1, MCP-1, IL-6, IL-18, MMP-2, MMP-7, MMP-9, FGF-23, and uric acid), with consideration of potential confounders. Results: Median long-term PM_2.5 exposure was 6.2 µg/m³. Almost all participants had a normal renal function and median eGFR was 99.2 mL/min/1.73 m². PM_2.5 exposure was associated with 1.3% (95% CI 0.6, 2.0) higher eGFR per 2.03 µg/m³ (interquartile range, IQR). PM_2.5 exposure was also associated with elevated serum matrix metalloproteinase 2 (MMP-2) concentration, with 7.2% (95% CI 1.9, 12.8) higher MMP-2 per 2.03 µg/m³. There was a tendency towards an association between PM₁₀ and higher levels of uric acid, but no associations were found with the other biomarkers. Associations with other air pollutants were null or inconsistent. Conclusion: In this large general population sample at low exposure levels, we found a surprising association between PM_2.5 exposure and a higher renal filtration. It seems unlikely that particle function would improve renal function. However, increased filtration is an early sign of renal injury and may be related to the relatively healthy population at comparatively low exposure levels. Furthermore, PM_2.5 exposure was associated with higher serum concentrations of MMP-2, an early indicator of renal and cardiovascular pathology.

Long-term exposure to air pollution is associated with cardiovascular events. A main suggested mechanism is that air pollution accelerates the progression of atherosclerosis, yet current evidence is inconsistent regarding the association between air pollution and coronary artery and carotid artery atherosclerosis, which are well-established causes of myocardial infarction and stroke. We studied associations between low levels of long-term air pollution, coronary artery calcium (CAC) score, and the prevalence and area of carotid artery plaques, in a middle-aged population-based cohort. The Swedish CArdioPulmonary bioImage Study (SCAPIS) Gothenburg cohort was recruited during 2013-2017 and thoroughly examined for cardiovascular risk factors, including computed tomography of the heart and ultrasonography of the carotid arteries. In 5070 participants (age 50-64 years), yearly residential exposures to air pollution (PM_2.5, PM₁₀, PM_coarse, NO_x, and exhaust-specific PM_2.5 1990-2015) were estimated using high-resolution dispersion models. We used Poisson regression to examine associations between long-term (26 years' mean) exposure to air pollutants and CAC score, and prevalence of carotid artery plaques, adjusted for potential confounders. Among participants with carotid artery plaques, we also examined the association with plaque area using linear regression. Mean exposure to PM_2.5 was low by international standards (8.5 μg/m³). There were no consistent associations between long-term total PM_2.5 exposure and CAC score or presence of carotid artery plaques, but an association between total PM_2.5 and larger plaque area in participants with carotid plaques. Associations with traffic-related air pollutants were consistently positive for both a high CAC score and bilateral carotid artery plaques. These associations were independent of road traffic noise. We found stronger associations among men and participants with cardiovascular risk factors. The results lend some support to atherosclerosis as a main modifiable pathway between low levels of traffic-related ambient air pollution and cardiovascular disease, especially in vulnerable individuals.

Despite firm evidence for an association between long-term ambient air pollution exposure and cardiovascular morbidity and mortality, results from epidemiological studies on the association between air pollution exposure and atherosclerosis have not been consistent. We investigated associations between long-term low-level air pollution exposure and coronary atherosclerosis. We performed a cross-sectional analysis in the large Swedish CArdioPulmonary bioImaging Study (SCAPIS, n = 30 154), a random general population sample. Concentrations of total and locally emitted particulate matter <2.5 μm (PM_2.5), <10 μm (PM₁₀), and nitrogen oxides (NO_x) at the residential address were modelled using high-resolution dispersion models. We estimated associations between air pollution exposures and segment involvement score (SIS), coronary artery calcification score (CACS), number of non-calcified plaques (NCP), and number of significant stenoses, using ordinal regression models extensively adjusted for potential confounders. Median 10-year average PM_2.5 exposure was 6.2 μg/m³ (range 3.5-13.4 μg/m³). 51 % of participants were women and 51 % were never-smokers. None of the assessed pollutants were associated with a higher SIS or CACS. Exposure to PM_2.5 was associated with NCP (adjusted OR 1.34, 95 % CI 1.13, 1.58, per 2.05 μg/m³). Associations with significant stenoses were inconsistent. In this large, middle-aged general population sample with low exposure levels, air pollution was not associated with measures of total burden of coronary atherosclerosis. However, PM_2.5 appeared to be associated with a higher prevalence of non-calcified plaques. The results suggest that increased risk of early-stage atherosclerosis or rupture, but not increased total atherosclerotic burden, may be a pathway for long-term air pollution effects on cardiovascular disease.

Ambient air pollution remains the major environmental cause of disease. Accurate assessment of population exposure and small-scale spatial exposure variations over long time periods is essential for epidemiological studies. We estimated annual exposure to fine and coarse particulate matter (PM_2.5, PM₁₀), and nitrogen oxides (NO_x, NO₂) with high spatial resolution to examine time trends 2000‒2018, compliance with the WHO Air Quality Guidelines, and assess the health impact. The modelling area covered six metropolitan areas in Sweden with a combined population of 5.5 million. Long-range transported air pollutants were modelled using a chemical transport model with bias correction, and locally emitted air pollutants using source-specific Gaussian-type dispersion models at resolutions up to 50 × 50 m. The modelled concentrations were validated using quality-controlled monitoring data. Lastly, we estimated the reduction in mortality associated with the decrease in population exposure. The validity of modelled air pollutant concentrations was good (R² for PM_2.5 0.84, PM₁₀ 0.61, and NO_x 0.87). Air pollution exposure decreased substantially, from a population weighted mean exposure to PM_2.5 of 12.2 µg m⁻³ in 2000 to 5.4 µg m⁻³ in 2018. We estimated that the decreased exposure was associated with a reduction of 2719 (95% CI 2046–3055) premature deaths annually. However, in 2018, 65%, 8%, and 42% of residents in the modelled areas were still exposed to PM_2.5, PM₁₀, or NO₂ levels, respectively, that exceeded the current WHO Air Quality Guidelines for annual average exposure. This emphasises the potential public health benefits of reductions in air pollution emissions.

Objectives Increasing epidemiological and experimental evidence suggests that particle exposure is an environmental risk factor for chronic kidney disease (CKD). However, only a few case–control studies have investigated this association in an occupational setting. Hence, our objective was to investigate associations between particle exposure and CKD in a large cohort of Swedish construction workers. Methods We performed a retrospective cohort study in the Swedish Construction Workers’ Cohort, recruited 1971–1993 (n=286 089). A job-exposure matrix was used to identify workers exposed to nine different particulate exposures, which were combined into three main categories (inorganic dust and fumes, wood dust and fibres). Incident CKD and start of renal replacement therapy (RRT) were obtained from validated national registries until 2021 and analysed using adjusted Cox proportional hazards models. Results Exposure to inorganic dust and fumes was associated with an increased risk of CKD and RRT during working age (adjusted HR for CKD at age <65 years 1.15, 95% CI 1.05 to 1.26). The elevated risk did not persist after retirement age. Exposure to cement dust, concrete dust and diesel exhaust was associated with CKD. Elevated HRs were also found for quartz dust and welding fumes. Conclusions Workers exposed to inorganic particles seem to be at elevated risk of CKD and RRT. Our results are in line with previous evidence of renal effects of ambient air pollution and warrant further efforts to reduce occupational and ambient particle exposure.