The effect of climate anomalies and ambient air pollution on spontaneous miscarriage in Ghana: Evidence from a national cross-sectional survey

Ambient particulate matter has been associated consistently with an increased risk for mortality largely due to cardiovascular diseases.1 Although the relative risk estimates from epidemiological studies are small, they apply to almost the entire population of the United States. Consequently, exposure to ambient particles produces considerable burden of disease, and its mitigation offers the benefit of improving life expectancy.2 Articles see pp 941 and 949 Over the past decade, research has substantiated the understanding of the pathophysiological mechanisms linking ambient particles to the cardiovascular system3,4 once it was noted that ambient air pollution elicits systemic inflammatory responses in the general population.5 An update of the American Heart Association statement on air pollution and cardiovascular disease3 is under way. Mechanisms considered for active and secondhand smoke as well as ambient air pollution are strikingly similar.4,6,7 They include progression of atherosclerotic plaques to vulnerable forms, prothrombotic states, endothelial dysfunction, and altered autonomic nervous system control (Figure). Increased systemic oxidative stress is considered the key mechanism responsible for most of these pathophysiological changes. Increased risks for cardiovascular disease in general and coronary artery disease in particular have been documented for active and secondhand smoke as well as ambient particulate matter. Deep venous thrombosis has been added to this list recently.8 Figure. Overview on pathomechanism linking ambient air pollution,4 secondhand smoke,7 and active smoking to acute coronary syndromes. Nevertheless, the public health relevance of particulate matter in the light of the smoking literature remains hotly debated. Smokers are exposed to considerably higher cumulative doses of particulate matter than the general nonsmoking population. Mortality due to low doses of ambient particles may be considered counterintuitive compared with doses of particles tolerated by smoking individuals. A systematic assessment of the exposure-response function ranging from low doses of inhaled particles …

Prenatal ambient air pollutants exposure and the risk of stillbirth in Wuhan, central of China

BACKGROUNDAlthough spontaneous miscarriage is the most common complication of human pregnancy, potential contributing factors are not fully understood. Advanced maternal age has long been recognised as a major risk factor for miscarriage, being strongly related with fetal chromosomal abnormalities. The relation between paternal age and the risk of miscarriage is less evident, yet it is biologically plausible that an increasing number of genetic and epigenetic sperm abnormalities in older males may contribute to miscarriage. Previous meta-analyses showed associations between advanced paternal age and a broad spectrum of perinatal and paediatric outcomes. This is the first systematic review and meta-analysis on paternal age and spontaneous miscarriage.OBJECTIVE AND RATIONALEThe aim of this systematic review and meta-analysis is to evaluate the effect of paternal age on the risk of spontaneous miscarriage.SEARCH METHODSPubMed, Embase and Cochrane databases were searched to identify relevant studies up to August 2019. The following free text and MeSH terms were used: paternal age, father’s age, male age, husband’s age, spontaneous abortion, spontaneous miscarriage, abortion, miscarriage, pregnancy loss, fetal loss and fetal death. PRISMA guidelines for systematic reviews and meta-analysis were followed. Original research articles in English language addressing the relation between paternal age and spontaneous miscarriage were included. Exclusion criteria were studies that solely focused on pregnancy outcomes following artificial reproductive technology (ART) and studies that did not adjust their effect estimates for at least maternal age. Risk of bias was qualitatively described for three domains: bias due to confounding, information bias and selection bias.OUTCOMESThe search resulted in 975 original articles. Ten studies met the inclusion criteria and were included in the qualitative synthesis. Nine of these studies were included in the quantitative synthesis (meta-analysis). Advanced paternal age was found to be associated with an increased risk of miscarriage. Pooled risk estimates for miscarriage for age categories 30–34, 35–39, 40–44 and ≥45 years of age were 1.04 (95% CI 0.90, 1.21), 1.15 (0.92, 1.43), 1.23 (1.06, 1.43) and 1.43 (1.13, 1.81) respectively (reference category 25–29 years). A second meta-analysis was performed for the subgroup of studies investigating first trimester miscarriage. This showed similar pooled risk estimates for the first three age categories and a slightly higher pooled risk estimate for age category ≥45 years (1.74; 95% CI 1.26, 2.41).WIDER IMPLICATIONSOver the last decades, childbearing at later ages has become more common. It is known that frequencies of adverse reproductive outcomes, including spontaneous miscarriage, are higher in women with advanced age. We show that advanced paternal age is also associated with an increased risk of spontaneous miscarriage. Although the paternal age effect is less pronounced than that observed with advanced maternal age and residual confounding by maternal age cannot be excluded, it may have implications for preconception counselling of couples comprising an older aged male.

Ambient air pollution the risk of stillbirth: A prospective birth cohort study in Wuhan, China.

We agree with Culic’s argument (2015) that environmental influences on human health are complex and likely multifactorial. Exposure to indoor and ambient urban air pollution has been estimated to contribute to 7 million premature deaths each year, predominantly from cardiovascular and respiratory conditions (Lim et al. 2012). Associations between exposure and cardiovascular mortality and morbidity have been demonstrated for nitrogen dioxide, sulfur dioxide, ozone, carbon monoxide, and particulate matter (Brook et al. 2010), although the associations are strongest for fine and ultrafine particulate matter (Hoek et al. 2013). Air pollution is extremely complex and consists not of single components in isolation but rather combinations of components. These constituent components interact with one another in the environment, which may alter potential toxicity and the subsequent health impacts. Meteorological factors such as wind speed and direction, humidity, atmospheric pressure, and temperature play an important part both in determining an individual’s exposure to ambient air pollution and in affecting the concentrations, chemical composition, and clearance of elements of the air pollution mixture. This is particularly true for the secondary pollutant ozone, which has a strong relationship with season and temperature (Langrish et al. 2010b). We agree that, in assessing the impact of ambient air pollution on public health, it is important to assess the air pollution mixture as a whole. In our studies we used a controlled exposure facility to assess, in a robust and well-validated fashion (Langrish et al. 2010a), the contribution to potential arrhythmogenesis of individual air pollutants—diesel exhaust, wood smoke, ozone, and nitrogen dioxide—as well as ambient air pollution in Beijing, China (Langrish et al. 2014). Exposure to neither air pollutants in isolation nor ambient Beijing air pollution was associated with cardiac dysrhythmia in either patients with coronary heart disease or healthy volunteers. As such, our studies do not address the influence of meteorological conditions on an individual’s risk of cardiac arrhythmia; indeed, the meteorological conditions in Beijing were fairly constant throughout our studies (Langrish et al. 2009, 2012). There is emerging evidence that cardiovascular morbidity and mortality is associated with meteorological and environmental conditions, and we agree with Culic’s statement that further research on the health impacts of atmospheric factors is important both for public health and for better understanding the interaction between urban air pollution and external influences.

Ambient air pollution in critical windows of exposure and spontaneous miscarriage in a preconception cohort.

Roles of pollution in the prevalence and exacerbations of allergic diseases in Asia

Study question What is the association between paternal lifestyle ­factors in the preconception period and the risk of spontaneous miscarriage? Summary answer Preconception paternal cigarette smoking is associated with an increased risk of spontaneous miscarriage, while no associations were found with paternal alcohol consumption and obesity. What is known already Although maternal lifestyle risk factors for miscarriage are well-established, studies on potentially contributing paternal factors remain sparse. Recently, a significant association was found between advanced paternal age and spontaneous miscarriage. Biological evidence indicates that smoking, excessive alcohol consumption and obesity may lead to sperm oxidative DNA damage, being a known risk factor for miscarriage. Study design, size, duration Systematic review and meta-analysis. Participants/materials, setting, methods PubMed and Embase databases were searched in August 2020. Paternal factors examined were: cigarette smoking, alcohol consumption and Body Mass Index (BMI). A qualitative risk of bias assessment was performed for all included studies. Meta-analysis was performed if sufficient data was available from studies that controlled for maternal factors. PRISMA guidelines for systematic reviews were followed. Main results and the role of chance The systematic search included 3386 articles of which 11 articles met the inclusion criteria. In a meta-analysis of eight studies, paternal smoking of > 10 cigarettes per day in the preconception period was found to be associated with an increased risk of spontaneous miscarriage, after adjustment for maternal smoking status (1-10 cigarettes per day: 1.01, 95% CI 0.97-1.06; 11-20 cigarettes per day: 1.12, 95% CI 1.08-1.16; >20 cigarettes per day: 1.23, 95% CI 1.17-1.29). Based on five available studies, no clear association was found between paternal alcohol consumption and spontaneous miscarriage. No studies were retrieved that evaluated the association between paternal BMI and spontaneous miscarriage. Limitations, reasons for caution Investigating the relation between paternal lifestyle factors and spontaneous miscarriage is challenging and prone to different forms of bias, especially in retrospective studies. Wider implications of the findings Awareness of the association between heavy paternal smoking in the preconception period and the risk of spontaneous miscarriage should be raised. More well-designed studies are needed to further investigate the effects of other paternal lifestyle factors on the risk of spontaneous miscarriage. Trial registration number not applicable

Study question What is the association between paternal lifestyle factors in the preconception period and the risk of spontaneous miscarriage? Summary answer: Preconception paternal cigarette smoking is associated with an increased risk of spontaneous miscarriage, while no associations were found with paternal alcohol consumption and obesity. What is known already Although maternal lifestyle risk factors for miscarriage are well-established, studies on potentially contributing paternal factors remain sparse. Recently, a significant association was found between advanced paternal age and spontaneous miscarriage. Biological evidence indicates that smoking, excessive alcohol consumption and obesity may lead to sperm oxidative DNA damage, being a known risk factor for miscarriage. Study design, size, duration: Systematic review and meta-analysis. Participants/materials, setting, methods PubMed and Embase databases were searched in August 2020. Paternal factors examined were: cigarette smoking, alcohol consumption and Body Mass Index (BMI). A qualitative risk of bias assessment was performed for all included studies. Meta-analysis was performed if sufficient data was available from studies that controlled for maternal factors. PRISMA guidelines for systematic reviews were followed. Main results and the role of chance The systematic search included 3386 articles of which 11 articles met the inclusion criteria. In a meta-analysis of eight studies, paternal smoking of > 10 cigarettes per day in the preconception period was found to be associated with an increased risk of spontaneous miscarriage, after adjustment for maternal smoking status (1–10 cigarettes per day: 1.01, 95% CI 0.97–1.06; 11–20 cigarettes per day: 1.12, 95% CI 1.08–1.16; >20 cigarettes per day: 1.23, 95% CI 1.17–1.29). Based on five available studies, no clear association was found between paternal alcohol consumption and spontaneous miscarriage. No studies were retrieved that evaluated the association between paternal BMI and spontaneous miscarriage. Limitations, reasons for caution Investigating the relation between paternal lifestyle factors and spontaneous miscarriage is challenging and prone to different forms of bias, especially in retrospective studies. Wider implications of the findings: Awareness of the association between heavy paternal smoking in the preconception period and the risk of spontaneous miscarriage should be raised. More well-designed studies are needed to further investigate the effects of other paternal lifestyle factors on the risk of spontaneous miscarriage. Trial registration number Not applicable

Numerous epidemiological studies report consistent associations between exposure to urban air pollution and cardio-respiratory morbidity and mortality. One of the important discoveries of these epidemiological studies during the last decade was that the increased mortality associated with enhanced air pollution exposure was not due only to pulmonary diseases, but mainly to cardiovascular diseases. (Zanobetti et al. 2003, Samet et al. 2000, Dockery et al. 1993, Jerrett et al. 2005, Pope et al. 2004a, Pope et al. 2002, Simkhovich, Kleinman and Kloner 2008, Nawrot, Nemmar and Nemery 2006, Hoek et al. 2002, Katsouyanni et al. 2001, Dominici et al. 2003). The focus in the initial epidemiological research was directed towards the association between both short-term and long-term exposure to air pollution and arterial cardiovascular effects, such as myocardial infarction. These landmark studies, in the beginning of the 90's, were quickly followed by experimental studies in humans and in rodents, to unravel the underlying pathophysiological mechanisms. The number of publications in this field increased exponentially, so that by the beginning of 2011, a search through PubMed using the MeSH terms 'air pollution' and 'cardiovascular disease' retrieved almost 1300 hits. Ambient environmental air pollutants include gaseous (carbon monoxide, nitrogen oxides, sulfur dioxide, ozone) and particulate components. The particulate component, particulate matter (PM), is subdivided based on size ranges into 'thoracic particles' (PM10, with a mean aerodynamic diameter 2.5 μm and <10 μm), 'fine particles' (PM2.5, <2.5 μm), and ultra-fine particles (UFP, <0.1 μm). Although exposure to some gaseous components has been linked to cardiovascular events, the larger body of evidence points towards the deleterious effects of the particulates in air pollution. Therefore, this chapter will focus mainly on the cardiovascular morbidity induced by PM exposure. Active cigarette smoking has been established as a major independent cause of cardiovascular disease (HHS 2004). The inhaled dose of fine particles from ambient air pollution, as from secondhand cigarette smoke, is extremely small compared with that from active cigarette smoking. Accordingly, the estimated relative risks from active smoking, even at relatively light smoking levels, are substantially larger than the risks from ambient air pollution or secondhand smoke. However, the risks induced by these latter 2 types of exposure are higher than would be expected from a simple linear extrapolation based on the amount of inhaled PM from active smoking (Pope et al. 2009), and have important public health implications (Nawrot et al. 2011).

We examined the association between ambient air pollution exposure and risk of spontaneous abortion (SAB) using Georgia state-wide fetal death records from 2005-2014. Each SAB case was matched to four non-SAB pregnancies by maternal residential county and conception month. Daily concentrations of ten pollutants were estimated and linked to maternal residential census tracts. Cox regression was used to estimate hazard ratios (HR) across four prenatal exposure windows (first month, weekly, cumulative weekly average over the first trimester, cumulative weekly average over the second trimester). Our dataset contained 47,649 SABs with a median gestational age of nine weeks. Carbon monoxide (CO) showed the strongest association, with an HR of 1.12 (1.05, 1.20) per 0.43 ppm increase in average first month exposure, and 1.06 (1.02, 1.10) per 0.42 ppm increase in average weekly exposure. Nitrogen dioxide (NO2) also exhibited elevated HRs. Other pollutants like nitrate compounds (NO3), nitrogen oxides (NOx), and organic carbon (OC) showed positive associations, while ozone (O3), PM2.5, PM10, elemental carbon (EC), and ammonium ions (NH4) were null. Early pregnancy exposure to traffic-related pollutants may increase SAB risk, highlighting potential benefits of air pollution regulation.

Air pollution in Hanoi, Vietnam : evaluating effects on hospital admissions of children

The associations between ambient air pollutants and tuberculosis seasonality are unclear. We assessed the temporal cross-correlations between ambient air pollutants and tuberculosis seasonality. Monthly tuberculosis incidence data and ambient air pollutants (PM2.5, PM10, carbon monoxide (CO), nitrogen dioxide (NO2), ozone (O3), sulfur dioxide (SO2)) and air quality index (AQI) from 2013 to 2017 in Shanghai were included. A cross-correlogram and generalized additive model were used. A 4-month delayed effect of PM2.5 (0.55), PM10 (0.52), SO2 (0.47), NO2 (0.40), CO (0.39), and AQI (0.45), and a 6-month delayed effect of O3 (−0.38) on the incidence of tuberculosis were found. The number of tuberculosis cases increased by 8%, 4%, 18%, and 14% for a 10 μg/m3 increment in PM2.5, PM10, SO2, and NO2; 4% for a 10 unit increment in AQI; 8% for a 0.1 mg/m3 increment in CO; and decreased by 4% for a 10 μg/m3 increment in O3. PM2.5 concentrations above 50 μg/m3, 70 μg/m3 for PM10, 16 μg/m3 for SO2, 47 μg/m3 for NO2, 0.85 mg/m3 for CO, and 85 for AQI, and O3 concentrations lower than 95 μg/m3 were positively associated with the incidence of tuberculosis. Ambient air pollutants were correlated with tuberculosis seasonality. However, this sort of study cannot prove causality.

Introduction: The impact of ambient air pollution (AAP) exposure on miscarriage is unclear. This study aims to examine AAP exposure on the risk of miscarriage and to investigate the critical window of exposure.Methods: A total of 201 women in early pregnancy (4-6 weeks) were recruited in this prospective cohort from Beijing during May 2016 to May 2017, and 178 were followed during the second and the third trimesters, and at delivery. The participants provided residential and demographic information, disease history, health habits, and occupational exposures in the baseline survey. Events of miscarriage including spontaneous abortion and embryonic loss were self-reported during the follow-up periods. AAP including particulate matter 2.5 (PM2.5), nitrogen dioxide (NO2), and ozone (O3) from the 35 monitoring stations in Beijing were collected. Land Use Regression model estimated the participants&amp;#8217; biweekly spatial AAP exposure from 8 weeks before conception till 20 weeks after. Log-binomial regression was used to assess the association of AAP exposure with the risk of miscarriage adjusted for parental age, maternal body mass index at baseline, and history of miscarriage or abortion.Results: A total of 22 (12.4%) participants reported miscarriage during 6-20 weeks of their pregnancy. APP exposure varied across the time period with ranges of 20.9 &amp;#8211; 207.6 ug/m3 for PM2.5, 10.7 - 109.0 ug/m3 for NO2, and 11.8 - 165.7 ug/m3 for O3. The risk of miscarriage was about 4 times higher (risk ratio &amp;#61; 3.85, 95% confidence interval: 1.13 - 13.25) in women exposed to the highest tertile of PM2.5 (Median: 74.2, Interquartile range[IQR]: 35.81) compared to women exposed to the lowest tertile of PM2.5 (Median:55.87, IQR: 4.69) during the first two weeks of pregnancy. Risk of miscarriage was not significantly associated with AAP exposures during other periods.Conclusion: Exposure to high level of PM2.5 during the first two weeks of pregnancy may increase the risk of miscarriage.

Air pollution has been examined in relation to stillbirth in few studies with inconsistent findings. No prior studies have examined the interaction of maternal asthma, a common pregnancy complication, and air pollution in relation to stillbirth risk. Our retrospective cohort analysis of 223,375 singleton deliveries, ≥23 weeks of gestation, from 12 clinical sites across the United States utilized electronic medical records. Average exposure to criteria air pollutants was calculated by modified Community Multiscale Air Quality models for the week prior to delivery, whole pregnancy and the first trimester. Poisson regression with generalized estimating equations estimated the relative risk (RR) of stillbirth and 95% confidence intervals in relation to an interquartile range (IQR) increase in pollutant after adjustment for age, race, parity, smoking, alcohol, pre-pregnancy body mass index, insurance, marital status, hypertension, diabetes, season of conception, birth year and study site. Maternal asthma was included with an interaction term to assess potential risk differences by asthma status. We observed 88 stillbirths among asthmatics (n=16,948, 0.52%) and 904 among non-asthmatics (n=205,435, 0.44%; p=0.14). Asthma significantly modifies the stillbirth risk (interaction p&lt;0.05) associated with an IQR increase in whole pregnancy particulate matter &lt;2.5 µm (PM2.5; RR=1.16 vs. 1.10), and first trimester average exposure to PM2.5 (RR=1.07 vs. 0.98), sulfur dioxide (RR=0.97 vs. 0.87), nitrogen oxides (RR=0.97 vs. 0.90) and carbon monoxide (CO; RR=1.09 vs. 0.92). Effect modification by asthma was not significant for ozone and PM &lt;10 µm, although ozone had a main effect on stillbirth. Acute exposure risk in the week prior to delivery also did not differ by asthma status. Despite low power due to a small number of cases, our findings suggest that PM2.5 and CO exposure could differentially increase stillbirth risk for asthmatic women and merit further investigation.