Association of anaemia with indoor air pollution among older Indian adult population: multilevel modelling analysis of nationally representative cross-sectional study.

INTRODUCTION: Anaemia is a disease of public health importance with multi-causal pathways. Previous literature suggests the role of indoor air pollution (IAP) on haemoglobin levels, but this has been studied less due to logistic constraints. A high proportion of the population in developing countries, including India, still depends on unclean fuel, which exacerbates IAP. The objective was to study the association between anaemia and IAP among the older Indian adult population (≥ 45 years) as per gender. METHODS: Our study analysed the nationally representative dataset of the Longitudinal Ageing Study in India (LASI 2017-18, Wave-1). We have documented the association of anaemia (outcome variable) with IAP (explanatory variable). To reduce the confounding effects of demographic and socioeconomic; health related and behavioural covariates; propensity score matching (PSM) was conducted. Nested multilevel regression modelling was conducted. States and union territories were categorised cross tabulated as low, middle and high as per anaemia and IAP exposure. P value < 0.05 was considered statistically significant. SATA version 17 was used for analysis. RESULTS: More than half (52.52%) of the participants were exposed to IAP (male (53.55%) > female (51.63%)). The odds of having anaemia was significantly 1.19 times higher (AOR 1.19 (1.09-1.31)) among participants using unclean/ solid fuel. The adjusted odds were significantly higher among participants exposed to pollution-generating sources (AOR 1.30; 1.18-1.43), and household indoor smoking (AOR 1.17 (1.07-1.29). The odds of having anaemia were significantly higher (AOR 1.26; 1.15-1.38) among participants exposed to IAP, which was higher in males (AOR 1.36; 1.15-1.61) than females (AOR 1.21; 1.08-1.35). Empowered Action Group (EAG) states like Uttar Pradesh, Chhattisgarh, Madhya Pradesh, Bihar had both high anaemia and IAP exposure. CONCLUSION: This study established the positive association of anaemia with indoor air pollution among older Indian adults through a nationally representative large dataset. The association was higher among men. Further research is recommended to understand detailed causation and to establish temporality. It is a high time to implement positive intervention nationally to decrease solid/ unclean fuel usage, vulnerable ventilation, indoor smoking, IAP and health hazards associated with these with more focused actions towards EAG states.

Association between exposure to smoke from cooking fuels and anaemia among women of reproductive age in Ghana.

In low- and middle-income countries, indoor air pollution (IAP) is a serious public health concern, especially for women and children who cook with solid fuels. IAP exposure has been linked to a number of medical conditions, including pneumonia, ischemic heart disease, stroke, chronic obstructive pulmonary disease (COPD), lung cancer, and anaemia. Around 500 million women of reproductive age (WRA) suffer from anaemia globally, with an estimated 190 million cases in sub-Saharan Africa (SSA). This study, which is based on prior research, investigates the relationship between IAP exposure and anaemia among WRA in Ghana. A diverse sample of 2,406 WRA living in Ghana were interviewed, of which 58.06% were anaemic and used high-pollutant fuels for cooking. Age, place of residence, region, education level, religion, ethnicity, wealth index, type of drinking water, type of toilet facility, and type of cooking fuels were all found to be significantly linked with anaemic state by bivariate analysis. Type of cooking fuels utilized, age, region of residence, and the type of residence were shown to be significant predictors of anaemia status using sequential binary logit regression models. The results emphasise the critical need for efforts to promote the usage of clean cooking fuel in an attempt to lower anaemia prevalence in Ghana. To reduce dependency on solid fuels for cooking, initiatives should promote the use of cleaner cooking fuels and enhance the socioeconomic status of households. These interventions could have significant public health effects by reducing the burden of anaemia and improving maternal and child health outcomes due to the prevalence of anaemia among WRA. Overall, this study sheds light on the relationship between IAP exposure and anaemia in Ghana and highlights the demand for focused public health initiatives to address this serious health problem.

Population attributable fractions of cancer mortality related to indoor air pollution, animal contact, and water source as environmental risk factors: Findings from the Golestan Cohort Study.

BACKGROUND: Environmental risk factors are significant contributors to cancer mortality, which are neglected. PURPOSE: This study aimed to estimate the population attributable fraction of cancer mortality due to the environmental risk factors. METHODS: Golestan cohort study is a population-base cohort on 50045 participants between 40-75 with about 18 years of follow up. We detected 2,196 cancer mortality and applied a multiple Cox model to compute the hazard ratio of environmental risk factor on all cancer and cancer-specific mortality. The population attributable fraction was calculated, accordingly. RESULTS: Biomass fuels for cooking, as an indoor air pollution, increased the risk of colorectal, esophageal, gastric cancer, and all-cancer mortality by 84%, 66%, 37%, and 17% respectively. Using gas for cooking, particularly in rural areas, could save 6% [Population Attributable Fraction: 6.36(95%CI: 1.82, 10.70)] of esophageal cancer, 3% [Population Attributable Fraction: 3.43 (0, 7.33)] of gastric cancer, and 6% [Population Attributable Fraction: 6.25 (1.76, 13.63)] of colorectal cancer mortality. Using a healthy tap water source could save 5% [Population Attributable Fraction:5.50(0, 10.93)] of esophageal cancer mortality, particularly in rural areas. There was no significant association between indoor air pollution for heating purposes and animal contact with cancer mortality. CONCLUSION: Considering the results of this study, eliminating solid fuel for most daily usage, among the population with specific cancer types, is required to successfully reduce cancer related mortality. Adopting appropriate strategies and interventions by policymakers such as educating the population, allocating resources for improving the healthy environment of the community, and cancer screening policies among susceptible populations could reduce cancer related mortalities.

Gas6-Axl signal promotes indoor VOCs exposure-induced pulmonary fibrosis via pulmonary microvascular endothelial cells-fibroblasts cross-talk.

Volatile organic compounds (VOCs) as environmental pollutants were associated with respiratory diseases. Pulmonary fibrosis (PF) was characterized by an increase of extracellular matrix, leading to deterioration of lung function. The adverse effects on lung and the potential mechanism underlying VOCs induced PF had not been elucidated clearly. In this study, the indoor VOCs exposure mouse model along with an ex vivo biosensor assay was established. Based on scRNA-seq analysis, the adverse effects on lung and potential molecular mechanism were studied. Herein, the results showed that VOCs exposure from indoor decoration contributed to decreased lung function and facilitated pulmonary fibrosis in mice. Then, the whole lung cell atlas after VOCs exposure and the heterogeneity of fibroblasts were revealed. We explored the molecular interactions among various pulmonary cells, suggesting that endothelial cells contributed to fibroblasts activation in response to VOCs exposure. Mechanistically, pulmonary microvascular endothelial cells (MPVECs) secreted Gas6 after VOCs-induced PANoptosis phenotype, bound to the Axl in fibroblasts, and then activated fibroblasts. Moreover, Atf3 as the key gene negatively regulated PANoptosis phenotype to ameliorate fibrosis induced by VOCs exposure. These novel findings provided a new perspective about MPVECs could serve as the initiating factor of PF induced by VOCs exposure.

Exploring the Cellular Impact of Size-Segregated Cigarette Aerosols: Insights into Indoor Particulate Matter Toxicity and Potential Therapeutic Interventions.

Exposure to anthropogenic aerosols has been associated with a variety of adverse health effects, increased morbidity, and premature death. Although cigarette smoke poses one of the most significant public health threats, the cellular toxicity of particulate matter contained in cigarette smoke has not been systematically interrogated in a size-segregated manner. In this study, we employed a refined particle size classification to collect cigarette aerosols, enabling a comprehensive assessment and comparison of the impacts exerted by cigarette aerosol extract (CAE) on SH-SY5Y, HEK293T, and A549 cells. Exposure to CAE reduced cell viability in a dose-dependent manner, with organic components having a greater impact and SH-SY5Y cells displaying lower tolerance compared to HEK293T and A549 cells. Moreover, CAE was found to cause increased oxidative stress, mitochondrial dysfunction, and increased levels of apoptosis, pyroptosis, and autophagy, leading to increased cell death. Furthermore, we found that rutin, a phytocompound with antioxidant potential, could reduce intracellular reactive oxygen species and protect against CAE-triggered cell death. These findings underscore the therapeutic potential of antioxidant drugs in mitigating the adverse effects of cigarette aerosol exposure for better public health outcomes.

Exposure to indoor air pollution and adverse pregnancy outcomes in low and middle-income countries: a systematic review and meta-analysis.

Introduction: Exposure to indoor air pollution such as biomass fuel and particulate matter is a significant cause of adverse pregnancy outcomes. However, there is limited information about the association between indoor air pollution exposure and adverse pregnancy outcomes in low and middle-income countries. Therefore, this meta-analysis aimed to determine the association between indoor air pollution exposure and adverse pregnancy outcomes in low and middle-income countries. Methods: International electronic databases such as PubMed, Science Direct, Global Health, African Journals Online, HINARI, Semantic Scholar, and Google and Google Scholar were used to search for relevant articles. The study was conducted according to the updated Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines. A random effect model at a 95% confidence interval was used to determine the association between indoor air pollution exposure and adverse pregnancy outcomes using STATA version 14. Funnel plot and Higgs I2 statistics were used to determine the publication bias and heterogeneity of the included studies, respectively. Results: A total of 30 articles with 2,120,228 study participants were included in this meta-analysis. The pooled association between indoor air pollution exposure and at least one adverse pregnancy outcome was 15.5% (95%CI: 12.6-18.5), with significant heterogeneity (I2 = 100%; p < 0.001). Exposure to indoor air pollution increased the risk of small for gestational age by 23.7% (95%CI: 8.2-39.3) followed by low birth weight (17.7%; 95%CI: 12.9-22.5). Exposure to biomass fuel (OR = 1.16; 95%CI: 1.12-1.2), particulate matter (OR = 1.28; 95%CI: 1.25-1.31), and kerosene (OR = 1.38; 95%CI: 1.09-1.66) were factors associated with developing at least one adverse pregnancy outcomes. Conclusions: We found that more than one in seven pregnant women exposed to indoor air pollution had at least one adverse pregnancy outcome. Specifically, exposure to particulate matter, biomass fuel, and kerosene were determinant factors for developing at least one adverse pregnancy outcome. Therefore, urgent comprehensive health intervention should be implemented in the area to reduce adverse pregnancy outcomes.

Association between exposure to airborne trichloramine and health effects in indoor swimming pool workers.

OBJECTIVE: The main objective of this study was to comprehensively investigate the association between trichloramine (TCA) exposure and respiratory health effects in swimming pool workers. METHODOLOGY: In this study, air sampling was performed for TCA concentrations at fixed locations (static measurements) and on individual workers (personal measurements) in six indoor public swimming pools during periods of high swimmer attendance over the winter school break. Health effects were evaluated using questionnaires and fractional exhaled nitric oxide (FENO) tests performed before and after the working day. RESULTS: In these swimming pools, the environmental TCA concentration ranged from 0.11 to 0.88 mg/m³. Worker exposure ranged from 0.05 to 0.72 mg/m³ for personal measurements. Furthermore, in each swimming pool, the average worker exposure to TCA exceeded the recommended occupational exposure limit of 0.35 mg/m³. Personal TCA measurements were consistently lower than static measurements performed around the pool, with a reduction ranging from 21% to 49%. This can be explained by the time that the workers spend in the pool area, office, and break room. The most common respiratory health effects self-reported by the workers were coughing, shortness of breath, and sneezing with prevalence rates of 38%, 37%, and 35%, respectively. This study demonstrated an association between TCA exposure and eye irritation. Analysis of the FENO tests revealed that individuals with preexisting asthma or allergies exhibited sustained FENO elevation. CONCLUSION: The findings suggest that occupational exposure to TCA in indoor swimming pools is a matter of concern. Implementing and improving workplace safety measures is crucial for safeguarding the respiratory health of swimming pool workers.

Everyday home radon exposure is associated with altered structural brain morphology in youths.

The refinement of brain morphology extends across childhood, and exposure to environmental toxins during this period may alter typical trends. Radon is a highly common radiologic toxin with a well-established role in cancer among adults. However, effects on developmental populations are understudied in comparison. This study investigated whether home radon exposure is associated with altered brain morphology in youths. Fifty-four participants (6-14 yrs, M=10.52 yrs, 48.15% male, 89% White) completed a T1-weighted MRI and home measures of radon. We observed a significant multivariate effect of home radon concentrations, which was driven by effects on GMV. Specifically, higher home radon was associated with smaller GMV (F=6.800, p=.012, ηp2=.13). Conversely, there was a trending radon-by-age interaction on WMV, which reached significance when accounting for the chronicity of radon exposure (F=4.12, p=.049, ηp2=.09). We found that youths with above-average radon exposure showed no change in WMV with age, whereas low radon was linked with normative, age-related WMV increases. These results suggest that everyday home radon exposure may alter sensitive structural brain development, impacting developmental trajectories in both gray and white matter.

Children's food allergy: Effects of environmental influences and antibiotic use across critical developmental windows.

BACKGROUND: Increasing studies linked outdoor air pollution (OAP), indoor environmental factors (IEFs), and antibiotics use (AU) with the first wave of allergies (i.e., asthma, allergic rhinitis, and eczema), yet the role of their exposures on children's second wave of allergy (i.e., food allergy) are unknown. OBJECTIVES: To investigate the association between exposure to OAP and IEFs and childhood doctor-diagnosed food allergy (DFA) during the pre-pregnancy, prenatal, early postnatal, and current periods, and to further explore the effect of OAP and IEFs on DFA in children co-exposed to antibiotics. METHODS: A retrospective cohort study involving 8689 preschoolers was carried out in Changsha, China. Data on the health outcomes, antibiotic use, and home environment of each child were collected through a questionnaire. Temperature and air pollutants data were obtained from 8 and 10 monitoring stations in Changsha, respectively. Exposure levels to temperature and air pollutants at individual home addresses were calculated by the inverse distance weighted (IDW) method. Multiple logistic regression models were employed to assess the associations of childhood DFA with exposure to OAP, IEF, and AU. RESULTS: Childhood ever doctor-diagnosed food allergy (DFA) was linked to postnatal PM10 exposure with OR (95% CI) of 1.18 (1.03-1.36), especially for CO and O3 exposure during the first year with ORs (95% CI) = 1.08 (1.00-1.16) and 1.07 (1.00-1.14), as well as SO2 exposure during the previous year with OR (95% CI) of 1.13 (1.02-1.25). The role of postnatal air pollution is more important for the risk of egg, milk and other food allergies. Renovation-related IAP (new furniture) and dampness-related indoor allergens exposures throughout all time windows significantly increased the risk of childhood DFA, with ORs ranging from 1.23 (1.03-1.46) to 1.54 (1.29-1.83). Furthermore, smoke-related IAP (environmental tobacco smoke [ETS], parental and grandparental smoking) exposure during pregnancy, first year, and previous year was related to DFA. Additionally, exposure to pet-related indoor allergens (cats) during first year and total plant-related allergens (particularly nonflowering plants) during previous year were associated with DFA. Moreover, exposure to plant-related allergy during first and previous year was specifically associated with milk allergy, while keeping cats during first year increased the risk of fruits/vegetables allergy. Life-time and early-life AU was associated with the increased risk of childhood DFA with ORs (95% CI) = 1.57 (1.32-1.87) and 1.46 (1.27-1.67), including different types food allergies except fruit/vegetable allergy. CONCLUSIONS: Postnatal OAP, life-time and early-life IEFs and AU exposure played a vital role in the development of DFA, supporting the "fetal origin of childhood FA" hypothesis.

Interior decorative volatile organic compounds exposure induces sleep disorders through aberrant branched chain amino acid transaminase 2 mediated glutamatergic signaling resulting from a neuroinflammatory cascade.

Air pollution has been recognized as a contributing factor to sleep disorders (SD), which have been correlated with an elevated susceptibility to a variety of human diseases. Nevertheless, research has not definitively established a connection between SD and interior decorative volatile organic compounds (ID-VOCs), a significant indoor air pollutant. In this study, we employed a mouse model exposed to ID-VOCs to explore the impacts of ID-VOCs exposure on sleep patterns and the potential underlying mechanism. Of the 23 key compositions of ID-VOCs identified, aromatic hydrocarbons were found to be the most prevalent. Exposure to ID-VOCs in mice resulted in SD, characterized by prolonged wake fullness and decreased sleep during the light period. ID-VOCs exposure triggered neuroinflammatory responses in the suprachiasmatic nucleus (SCN), with microglia activation leading to the overproduction of inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1α (IL-1α), and complement component 1q (C1q), ultimately inducing A1 astrocytes. Consequently, the upregulation of branched chain amino acid transaminase 2 (BCAT2) in A1 astrocytes resulted in elevated extracellular glutamate and disruption of the wake-sleep transition mechanism, which might be the toxicological mechanism of SD caused by ID-VOCs.

Association between indoor air pollution and depression: a systematic review and meta-analysis of cohort studies.

OBJECTIVES: Incomplete combustion of solid fuel and exposure to secondhand smoke (SHS) are the primary causes of indoor air pollution (IAP), potentially leading to detrimental effects on individual mental health. However, current evidence regarding the association between IAP and depression remains inconclusive. This study aims to systematically investigate the evidence regarding the association between IAP and the risk of depression. DESIGN: Systematic review and meta-analysis of cohort studies. DATA SOURCES: Two independent reviewers searched PubMed, the Cochrane Library, Web of Science and EMBASE for available studies published up to 13 January 2024. ELIGIBILITY CRITERIA: We included all cohort studies published in English that aimed to explore the relationship between IAP from solid fuel use and SHS exposure and the risk of depression. DATA EXTRACTION AND SYNTHESIS: Two independent reviewers extracted data and assessed the risk of bias. The association between IAP and depression was calculated using pooled relative risk (RR) with 95% CIs. Heterogeneity was assessed using the I2 value, and the effect estimates were pooled using fixed-effects or random-effects models depending on the results of homogeneity analysis. RESULTS: We included 12 articles with data from 61 217 participants. The overall findings demonstrated a significant association between IAP exposure and depression (RR=1.22, 95% CI: 1.13 to 1.31), although with substantial heterogeneity (I2=75%). Subgroup analyses based on pollutant type revealed that IAP from solid fuel use was associated with a higher risk of depression (RR=1.20, 95% CI: 1.13 to 1.26; I2=62%; 5 studies, 36 768 participants) than that from SHS exposure (RR=1.11, 95% CI: 0.87 to 1.41; I2=80%; 7 studies, 24 449 participants). In terms of fuel use, the use of solid fuel for cooking (RR: 1.23, 95% CI: 1.16 to 1.31; I2=58%; 4 studies, 34 044 participants) and heating (RR 1.15, 95% CI: 1.04 to 1.27; I2=65%; 3 studies, 24 874 participants) was associated with increased depression risk. CONCLUSIONS: The findings from this systematic review and meta-analysis of cohort studies indicated an association between exposure to IAP and depression. PROSPERO REGISTRATION NUMBER: CRD42022383285.

Influence of type of cooking fuel on risk of hypertension among reproductive-age women in sub-Saharan Africa: insights from nationally representative cross-sectional surveys.

BACKGROUND: Nearly one-third of the world's population (2.4 billion people) rely on unclean cooking fuel sources. The study assessed the association of the type of cooking fuel and hypertension risk in sub-Saharan Africa (SSA). METHODS: The study analysed pooled data from 97 942 individuals in the Demographic and Health Survey (DHS) between 2014 and 2021 in 10 SSA countries. Univariate, bivariate and multivariate analyses were performed, including basic descriptive statistics and binary logistic regression. The independent variable of interest was the type of cooking fuel, while hypertension served as the outcome variable. RESULTS: Women using unclean cooking fuel were 1.21 times more likely to be hypertensive compared with those using clean cooking fuel (adjusted odds ratio [aOR] 1.21 [95% confidence interval {CI} 1.11 to 1.31]). Older age (aOR 5.78 [95% CI 5.04 to 6.62]), higher education (aOR 1.14 [95% CI 1.05 to 1.23]), being married (aOR 1.64 [95% CI 1.49 to 1.80]), working in sales and services occupations (aOR 1.34 [95% CI 1.24 to 1.44]), frequent health facility visits (aOR 1.59 [95% CI 1.51 to 1.68]), higher wealth index and exposure to media were significantly associated with hypertension risk. CONCLUSIONS: Efforts to reduce reliance on unclean cooking fuel at both the household and population levels need to be intensified in SSA countries. Promoting the use of clean cooking technologies and fuels and implementing supportive policies for transitioning from unclean cooking fuels are crucial. Targeted interventions to reduce hypertension risk in SSA should focus on women using unclean cooking fuel, older women, individuals from wealthier households and those with higher education levels.

Nitrogen dioxide exposure, health outcomes, and associated demographic disparities due to gas and propane combustion by U.S. stoves.

Gas and propane stoves emit nitrogen dioxide (NO2) pollution indoors, but the exposures of different U.S. demographic groups are unknown. We estimate NO2 exposure and health consequences using emissions and concentration measurements from >100 homes, a room-specific indoor air quality model, epidemiological risk parameters, and statistical sampling of housing characteristics and occupant behavior. Gas and propane stoves increase long-term NO2 exposure 4.0 parts per billion volume on average across the United States, 75% of the World Health Organization's exposure guideline. This increased exposure likely causes ~50,000 cases of current pediatric asthma from long-term NO2 exposure alone. Short-term NO2 exposure from typical gas stove use frequently exceeds both World Health Organization and U.S. Environmental Protection Agency benchmarks. People living in residences <800 ft2 in size incur four times more long-term NO2 exposure than people in residences >3000 ft2 in size; American Indian/Alaska Native and Black and Hispanic/Latino households incur 60 and 20% more NO2 exposure, respectively, than the national average.

Determining the toxicological effects of indoor air pollution on both a healthy and an inflammatory-comprised model of the alveolar epithelial barrier in vitro.

Exposure to indoor air pollutants (IAP) has increased recently, with people spending more time indoors (i.e. homes, offices, schools and transportation). Increased exposures of IAP on a healthy population are poorly understood, and those with allergic respiratory conditions even less so. The objective of this study, therefore, was to implement a well-characterised in vitro model of the human alveolar epithelial barrier (A549 + PMA differentiated THP-1 incubated with and without IL-13, IL-5 and IL-4) to determine the effects of a standardised indoor particulate (NIST 2583) on both a healthy lung model and one modelling a type-II (stimulated with IL-13, IL-5 and IL-4) inflammatory response (such as asthma).Using concentrations from the literature, and an environmentally appropriate exposure we investigated 232, 464 and 608ng/cm2 of NIST 2583 respectively. Membrane integrity (blue dextran), viability (trypan blue), genotoxicity (micronucleus (Mn) assay) and (pro-)/(anti-)inflammatory effects (IL-6, IL-8, IL-33, IL-10) were then assessed 24 h post exposure to both models. Models were exposed using a physiologically relevant aerosolisation method (VitroCell Cloud 12 exposure system).No changes in Mn frequency or membrane integrity in either model were noted when exposed to any of the tested concentrations of NIST 2583. A significant decrease (p < 0.05) in cell viability at the highest concentration was observed in the healthy model. Whilst cell viability in the "inflamed" model was decreased at the lower concentrations (significantly (p < 0.05) after 464ng/cm2). A significant reduction (p < 0.05) in IL-10 and a significant increase in IL-33 was seen after 24 h exposure to NIST 2583 (464, 608ng/cm2) in the "inflamed" model.Collectively, the results indicate the potential for IAP to cause the onset of a type II response as well as exacerbating pre-existing allergic conditions. Furthermore, the data imposes the importance of considering unhealthy individuals when investigating the potential health effects of IAP. It also highlights that even in a healthy population these particles have the potential to induce this type II response and initiate an immune response following exposure to IAP.

Household air pollution and urinary incontinence symptoms among older adults in LASI: a large-scale population-based study.

BACKGROUND: The effects of household air pollution on urinary incontinence (UI) symptoms and stress urinary incontinence (SUI) symptoms have not been studied. This study seeks to investigate the correlation between household air pollution and UI/SUI symptoms among middle-aged and elderly adults in India. METHODS: We employed data derived from individuals aged 45 years and older who participated in the inaugural wave (2017-2018) of the Longitudinal Aging Study in India (LASI). The assessment of household air pollution exposure and the occurrence of UI/SUI symptoms relied on self-reported data. The analytical approach adopted was cross-sectional in nature and encompassed a cohort of 64,398 participants. To explore relationships, we utilized multivariate logistic regression analysis, incorporating subgroup analysis and interaction tests. RESULTS: 1,671 (2.59%) participants reported UI symptoms and 4,862 (7.55%) participants reported SUI symptoms. Also, the prevalence of UI/SUI symptoms is much higher among middle-aged and elderly adults who use solid polluting fuels (UI: 51.23% vs. 48.77%; SUI: 54.50% vs. 45.50%). The results revealed a noteworthy correlation between household air pollution and the probability of experiencing UI/SUI symptoms, persisting even after adjusting for all conceivable confounding variables (UI: OR = 1.552, 95% CI: 1.377-1.749, p < 0.00001; SUI: OR: 1.459, 95% CI: 1.357-1.568, p < 0.00001). Moreover, significant interaction effects were discerned for age, education level, tobacco consumption, alcohol consumption, and physical activity (p for interaction < 0.05). CONCLUSIONS: The results of our study indicate that the utilization of solid fuels in the home increases the likelihood of developing urinary incontinence and stress urinary incontinence. As a result, we argue that there is an immediate need to reform the composition of cooking fuel and raise public awareness about the adverse effects of air pollution in the home.

Early life ambient air pollution, household fuel use, and under-5 mortality in Ghana.

INTRODUCTION: Environmental exposures, such as ambient air pollution and household fuel use affect health and under-5 mortality (U5M) but there is a paucity of data in the Global South. This study examined early-life exposure to ambient particulate matter with a diameter of 2.5 µm or less (PM2.5), alongside household characteristics (including self-reported household fuel use), and their relationship with U5M in the Navrongo Health and Demographic Surveillance Site (HDSS) in northern Ghana. METHODS: We employed Satellite-based spatiotemporal models to estimate the annual average PM2.5 concentrations with the Navrongo HDSS area (1998 to 2016). Early-life exposure levels were determined by pollution estimates at birth year. Socio-demographic and household data, including cooking fuel, were gathered during routine surveillance. Cox proportional hazards models were applied to assess the link between early-life PM2.5 exposure and U5M, accounting for child, maternal, and household factors. FINDINGS: We retrospectively studied 48,352 children born between 2007 and 2017, with 1872 recorded deaths, primarily due to malaria, sepsis, and acute respiratory infection. Mean early-life PM2.5 was 39.3 µg/m3, and no significant association with U5M was observed. However, Children from households using "unclean" cooking fuels (wood, charcoal, dung, and agricultural waste) faced a 73 % higher risk of death compared to those using clean fuels (adjusted HR = 1.73; 95 % CI: 1.29, 2.33). Being born female or to mothers aged 20-34 years were linked to increased survival probabilities. INTERPRETATION: The use of "unclean" cooking fuel in the Navrongo HDSS was associated with under-5 mortality, highlighting the need to improve indoor air quality by introducing cleaner fuels.

Prenatal risk factors of indoor environment and incidence of childhood eczema in the Japan Environment and Children's Study.

The quality of indoor environment is a risk factor for early childhood eczema and atopic dermatitis; however, its influence during pregnancy on childhood eczema in Japan has not been investigated. In this study, we aimed to determine the indoor environmental factors that are associated with eczema in children up to 3 years of age, using national birth cohort data from the Japan Environment and Children's Study (JECS). Information on indoor environments and eczema symptoms until 3 years of age was collected using self-administered questionnaires to the mothers. A total of 71,883 and 58,639 mother-child pairs at 1.5- and 3-years-old, respectively, were included in the former analyses. To account for prenatal indoor risk factors, 17,568 (1.5-years-old) and 7063 (3-years-old) children without indoor mold and/or ETS exposure were included in the final analysis. A higher mold index, gas heater use, parquet flooring use, and frequent insecticide use showed significantly increased risks for childhood eczema up to 3 years of age. These associations were consistent after stratification analysis among children whose parents did not have a history of allergies. The updated WHO guidelines on indoor air quality should be implemented based on recent findings regarding the effects of prenatal exposure to indoor dampness on health effects of children further in life, including asthma, respiratory effects, eczema, and other immunological effects.