Association between ambient particulate matter exposure and semen quality in fertile men.
Ontology highlight
ABSTRACT: Background
Several studies have suggested adverse effects of particulate matter (PM) exposure on male reproductive health; few have investigated the association between PM exposure and semen quality in a large population of fertile men.Methods
We evaluated 14 parameters of semen quality in 1554 fertile men in Nanjing from 2014 to 2016. Individual exposure to particular matter ≤10 μm in diameter (PM10) and ≤ 2.5 μm in diameter (PM2.5) during key periods of sperm development (0-90, 0-9, 10-14, 15-69, and 70-90 days before semen collection) were estimated by inverse distance weighting interpolation. Associations between PM exposure and semen quality were estimated using multivariable linear regression.Results
Higher 90-days average PM2.5 was in association with decreased sperm motility (2.21% for total motility, 1.93% for progressive motility per 10 μg/m3 increase, P < 0.001) and four quantitative aspects of sperm motion (curvilinear velocity (VCL), straight line velocity (VSL), average path velocity (VAP), and amplitude of lateral head displacement (ALH), P < 0.01). The association between PM2.5 exposure and semen quality were generally stronger for the earlier exposure window (70-90 days prior to ejaculation) than for recent exposure (0-9, 10-14, or 15-69 days). In the subgroup of men who had normal sperm parameters (n = 1019), similar results were obtained. Ninety-days PM10 exposure was associated only with decreased VCL and VAP and was not related to sperm concentration.Conclusions
Exposure to PM2.5 adversely affects semen quality, specifically lower sperm motility, in fertile men.
SUBMITTER: Wu W
PROVIDER: S-EPMC8762955 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:ImportanceThe health effects of exposure to particulate matter (PM) on male fertility remain unclear. Although PM exposure has been linked with semen quality, the results were inconsistent.ObjectiveTo examine the association of different size fractions of PM (<2.5 μm [PM2.5], 2.5-10 μm [PM2.5-10], and ≤10 μm [PM10]) exposure with semen quality in China.Design, setting, and participantsThis retrospective cohort study was conducted using data on men whose wives underwent assisted reproductive technology procedures in a tertiary hospital in Shanghai, China, from January 1, 2013, to December 31, 2019. Participants were from 340 prefecture-level cities of China and were followed up from the date of their first visit until December 31, 2019. Data were analyzed from December 1, 2020, to May 15, 2021.ExposuresExposure to PM2.5, PM2.5-10, and PM10 during the entire period (0-90 days before semen ejaculation) and key periods of sperm development (0-9, 10-14, and 70-90 days before semen ejaculation).Main outcomes and measuresSemen quality, including sperm count, concentration, and motility.ResultsA total of 33 876 men were included in the final analysis, with a mean (SD) age of 34.1 (5.7) years and large variation of PM exposure. For example, the median exposure to PM2.5 during the entire period of sperm development was 46.05 (IQR, 34.38-61.65) μg/m3. During the entire period of sperm development, exposures to higher levels of PM were significantly associated with lower total and progressive sperm motility. For total sperm motility, an IQR increase in PM2.5 exposure was associated with an estimated effect decrease of -3.60% (95% CI, -3.93% to -3.26%); an increase in PM2.5-10 exposure, with an estimated effect decrease of -0.45% (95% CI, -0.76% to -0.14%); and an increase in PM10 exposure, with an estimated effect decrease of -2.44% (95% CI, -2.91% to -1.96%). Similar results were observed for progressive motility. An IQR increase in PM2.5 or PM10 exposures was associated with an estimated effect decrease on sperm progressive motility of -1.87% (95% CI, -2.37% to -1.36%) and -1.05% (95% CI, -1.45% to -0.64%), respectively. However, no significant associations were observed between PM exposure during the entire period of sperm development and sperm count or concentration.Conclusions and relevanceThese findings suggest that PM exposure may adversely affect sperm motility and highlight the need to reduce ambient particulate air pollution exposure for reproductive-aged men.
| S-EPMC8855237 | biostudies-literature
Project description:Several experimental and observational studies have demonstrated the antiandrogenicity of several phthalates. However, there is limited evidence of an association between phthalate exposure in adult life and semen quality. The aim of this study was to examine phthalate exposure during adulthood in relation to semen quality in fertile US men. This multi-center cross-sectional study included 420 partners of pregnant women who attended a prenatal clinic in one of five US cities during 1999-2001. Nine phthalate metabolites [mono (2-ethylhexyl) phthalate (MEHP), mono (2-ethyl-5-hydroxyhexyl) phthalate (MEHHP), mono (2-ethyl-5-oxohexyl) phthalate (MEOHP), and mono (2-ethyl-5-carboxypentyl) phthalate (MECPP)], as well as mono-n-butyl phthalate (MBP) and mono-isobutyl phthalate (MiBP), mono (three carboxypropyl) phthalate (MCPP), monobenzyl phthalate (MBzP), and monoethyl phthalate (MEP)] were measured in urine collected at the same time as the semen sample. We regressed natural log-transformed (ln) sperm concentration, ln(total sperm count), ln(total motile sperm count), percent motile spermatozoa, and percent spermatozoa with normal morphology on each of the nine natural log-transformed metabolite concentrations and on the molar-weighted sum of DEHP metabolites in separate models. We fit unadjusted models and models that adjusted for confounders determined a priori. In unadjusted models, ln(MiBP) was significantly and positively associated with motility and ln(MBzP) significantly negatively associated with ln(total sperm count). In adjusted linear models, urinary metabolite concentrations of DEHP, DBP, DEP, and DOP were not associated with any semen parameter. We found an inverse association between ln(MBzP) concentrations and sperm motility (? = -1.47, 95% CI: -2.61, -0.33), adjusted for ln(creatinine concentration), geographic location, age, race, smoking status, stress, recent fever, time from sample collection and time to complete analysis. Several sensitivity analyses confirmed the robustness of these associations. This study and the available literature suggest that impacts of adult exposure to phthalates at environmental levels on classical sperm parameters are likely to be small.
| S-EPMC4879116 | biostudies-literature
Project description:Evidence concerning the association between ambient gaseous air pollutant exposures and semen quality is sparse, and findings in previous studies remain largely inconsistent. We enrolled 1759 men and performed 2184 semen examinations at a large reproductive medical center in Wuhan, China, between 2013 and 2015. Inverse distance weighting interpolation was performed to estimate individual exposures to SO2, NO2, CO, and O3 during the entire period (lag 0-90 days) and key periods (lag 0-9, 10-14, 70-90 days) of sperm development. Linear mixed models were used to analyze exposure-response relationships. SO2 exposure with 0-90 days lag was significantly associated with monotonically decreased sperm concentration (β for each interquartile range increase of exposure: -0.14; 95% CI: -0.23, -0.05), sperm count (-0.21; -0.30, -0.12) and total motile sperm count (-0.16; -0.25, -0.08). Significant associations were observed for total and progressive motility only when SO2 exposure was at the highest quintile (all Ptrend < 0.05). Similar trends were observed for SO2 exposure with 70-90 days lag. NO2, CO, or O3 exposure was not significantly associated with semen quality. Our results suggest that ambient SO2 exposure adversely affects semen quality and highlight the potential to improve semen quality by reducing ambient SO2 exposure during early stages of sperm development.
| S-EPMC5822717 | biostudies-literature
Project description:To establish a base line for future studies on temporal trends, to describe potential geographical differences in semen quality and reference values for studies of men from the general population. Cross-sectional study of fertile men from four areas in Japan. Inclusion criteria were: age 20-45 years at the time of invitation, and both the man and his mother had to be born in Japan. Additionally, the current pregnancy of the female partner had to be achieved by normal sexual relations without any fertility treatment. Four Japanese study centres at urban areas located in Sapporo, Osaka, Kanazawa and Fukuoka. 792 men, median age 31.4 years, included from 1999 to 2002. Semen volume, sperm concentration, total sperm count, sperm motility and sperm morphology. Semen volumes, percentages of motile spermatozoa and morphologically normal spermatozoa differed slightly between the four groups, whereas no differences in sperm concentrations or total sperm counts were found. In total, 1.2% of men had a sperm concentration below 5 million/ml, 2.1% below 10 million/ml, 3.5% below 15 million/ml and 16.3% below 40 million/ml. For morphology, 14.7% had less than 5% normal spermatozoa. Reproductive hormone levels varied significantly, however, only little from a biological point of view. This is the first cross-sectional study on semen quality covering fertile men from the major regions of Japan. It showed that semen quality of fertile Japanese men is comparable to that of the best in European regions. The results may serve as reference values for studies of men from the general population.
| S-EPMC3563117 | biostudies-literature
Project description:UnlabelledThe objective of this research was to determine if prenatal exposure to two common urban air pollutants, diesel and perchloroethylene, affects children's 3rd grade standardized test scores in mathematics and English language arts (ELA). Exposure estimates consisted of annual average ambient concentrations of diesel particulate matter and perchloroethylene obtained from the Environmental Protection Agency's 1996 National Air Toxics Assessment for the residential census tract at birth. Outcome data consisted of linked birth and educational records for 201,559 singleton, non-anomalous children born between 1994 and 1998 who attended New York City public schools. Quantile regression models were used to estimate the effects of these exposures on multiple points within the continuous distribution of standardized test scores. Modified Poisson regression models were used to calculate risk ratios (RR) and 95% confidence intervals (CI) of failing to meet curricula standards, an indicator derived from test scores. Models were adjusted for a number of maternal, neighborhood and childhood factors. Results showed that math scores were approximately 6% of a standard deviation lower for children exposed to the highest levels of both pollutants as compared to children with low levels of both pollutants. Children exposed to high levels of both pollutants also had the largest risk of failing to meet math test standards when compared to children with low levels of exposure to the pollutants (RR 1.10 95%CI 1.07,1.12 RR high perchloroethylene only 1.03 95%CI 1.00,1.06; RR high diesel PM only 1.02 95%CI 0.99,1.06). There was no association observed between exposure to the pollutants and failing to meet ELA standards. This study provides preliminary evidence of associations between prenatal exposure to urban air pollutants and lower academic outcomes. Additionally, these findings suggest that individual pollutants may additively impact health and point to the need to study the collective effects of air pollutant mixtures.Key wordsair toxics, academic outcomes, urban health, tetrachloroethylene, air pollutant mixtures.
| S-EPMC4874864 | biostudies-literature
Project description:BackgroundFetal growth has been known to be associated with particulate matter (PM) air pollution during gestation. Given that regular working may deviate outdoor air pollution exposure, the association between air pollution and fetal growth restriction can be different across maternal working status. This study was to assess possible effect modification by maternal employment in the association between exposure to PM during pregnancy and fetal growth restriction.MethodsUsing hourly PM less than or equal to 10 and 2.5??m in diameter (PM10 and PM2.5) regulatory monitoring data for 2001-2012 and 2008-2012, respectively, and birth certificate data for 2002-2012, we computed maternal exposures with district-level averages of PM10 and PM2.5 during one year before birth, entire pregnancy, and the 1st, 2nd and 3rd trimesters. The outcomes of fetal growth restriction were assessed by small for gestational age (SGA, weighted <10th percentile in the same gestational age) as well as low birth weight (LBW, <?2.5?kg) at term. We performed logistic regression to examine the association between PM and each of fetal growth restriction outcomes adjusting for individual risk factors. For effect modification by maternal employment, we estimated adjusted odds ratio (OR) of SGA or LBW for interquartile (IQR) increases in PM10 or PM2.5 stratified by employed and non-employed mothers. We also computed relative excess risk due to interaction (RERI) to investigate additive interaction.ResultsAmong 824,011 singleton term births, 34.0% (279,856) were employed and 66.0% (544,155) were non-employed mothers. Proportions of LBW were 1.5% in employed and 1.6% in non-employed (P <?0.001). SGA occurred in 12.7% of employed and 12.8% of non- employed (P =?0.124) mothers. For non-employed mothers, we observed increased odds of SGA per IQR increase in PM10 for one year before birth (OR?=?1.02, 95% confidence intervals (CI): 1.00-1.04, P =?0.028). ORs of SGA for full pregnancy period and the 3rd trimester were also positive but did not reach statistical significance. We did not observe positive association for PM2.5. RERI was not significant both for PM10 and PM2.5.ConclusionsWe did not observe evidence of effect modification by maternal employment in the association between ambient PM and fetal growth restriction. Future studies using more refined exposure measures should confirm this finding.
| S-EPMC6632189 | biostudies-literature
Project description:Epidemiologic and health impact studies are inhibited by the paucity of global, long-term measurements of the chemical composition of fine particulate matter. We inferred PM2.5 chemical composition at 0.1° × 0.1° spatial resolution for 2004-2008 by combining aerosol optical depth retrieved from the MODIS and MISR satellite instruments, with coincident profile and composition information from the GEOS-Chem global chemical transport model. Evaluation of the satellite-model PM2.5 composition data set with North American in situ measurements indicated significant spatial agreement for secondary inorganic aerosol, particulate organic mass, black carbon, mineral dust, and sea salt. We found that global population-weighted PM2.5 concentrations were dominated by particulate organic mass (11.9 ± 7.3 ?g/m(3)), secondary inorganic aerosol (11.1 ± 5.0 ?g/m(3)), and mineral dust (11.1 ± 7.9 ?g/m(3)). Secondary inorganic PM2.5 concentrations exceeded 30 ?g/m(3) over East China. Sensitivity simulations suggested that population-weighted ambient PM2.5 from biofuel burning (11 ?g/m(3)) could be almost as large as from fossil fuel combustion sources (17 ?g/m(3)). These estimates offer information about global population exposure to the chemical components and sources of PM2.5.
| S-EPMC4238642 | biostudies-literature
Project description:It is generally accepted that exposure to particulate matter (PM) increases the risk of cardiovascular-related morbidity and mortality, though the exact mechanism behind this has yet to be elucidated. Oxidative stress plays a potentially important role in the mechanism of toxicity, with Nrf2 serving as a major antioxidant gene. In the current study, a Nrf2 knockout mouse model was used in combination with an individual ventilated cage (IVC)-based real-ambient PM exposure system to assess the potential cardiotoxicity induced by real-ambient PM exposure and the potential role of Nrf2 and related signaling in this endpoint. After 6- or 11-weeks exposure to PM, ICP-mass spectrometry was used to assess the metal depositions in the heart tissue following PM exposure. Functional and morphological changes in the hearts were investigated with echocardiography and histopathology, and oxidative stress levels were assessed with a serum malondialdehyde content assay. In the further mechanistic study, an RNA-seq technique was utilized to assess the gene transcription status in the hearts of C57/B6 mice exposed to PM with or without Nrf2 knockout. The expression levels of genes of interest were then further investigated with quantitative real-time PCR and western blotting. The results indicated that PM exposure resulted in significant elevation of sodium, potassium, selenium, and ferrum levels in mouse heart tissue. Meanwhile, significantly altered heart function and morphology were observed. Interestingly, Nrf2 knockout led to abolishment of PM-induced effects in several functional parameters but not the morphological changes. Meanwhile, elevated malondialdehyde content was observed in Nrf2 knockout animals. RNA-seq results revealed thousands of genes altered by PM exposure and/or Nrf2 knockout, and this affected several pathways, such as MAPK, phagosome, calcium signaling, and JAK-STAT. In subsequent molecular studies, enhanced nuclear translocation of Nrf2 was also observed following PM exposure, while the MAPK signaling pathway along with related JAK-STAT and TGF-β1 pathway genes, such as p38MAPK, AKT, TAK1, JAK1, STAT3, GRB2, TGFb1, and SMAD2, were confirmed to be affected by PM exposure and/or Nrf2 knockout. The data suggested that PM may induce cardiotoxicity in C57/B6 mice in which Nrf2 plays both protective and detrimental roles involving cardiac-related pathways, such as MAPK, JAK-STAT, and TGF-β1.
| S-EPMC7136766 | biostudies-literature
Project description:Although numerous experimental studies have suggested a significant association between ambient particulate matter (PM) and respiratory damage, the etiological relationship between ambient PM and environmental skin diseases is not clearly understood. Here, we aimed to explore the association between PM and skin diseases through biological big data analysis. Differential gene expression profiles associated with PM and environmental skin diseases were retrieved from public genome databases. The co-expression among them was analyzed using a text-mining-based network analysis software. Activation/inhibition patterns from RNA-sequencing data performed with PM2.5-treated normal human epidermal keratinocytes (NHEK) were overlapped to select key regulators of the analyzed pathways. We explored the adverse effects of PM on the skin and attempted to elucidate their relationships using public genome data. We found that changes in upstream regulators and inflammatory signaling networks mediated by MMP-1, MMP-9, PLAU, S100A9, IL-6, and S100A8 were predicted as the key pathways underlying PM-induced skin diseases. Our integrative approach using a literature-based co-expression analysis and experimental validation not only improves the reliability of prediction but also provides assistance to clarify underlying mechanisms of ambient PM-induced dermal toxicity that can be applied to screen the relationship between other chemicals and adverse effects.
| S-EPMC9192598 | biostudies-literature
Project description:Murine Pulmonary Responses to Ambient Baltimore Particulate Matter: Genomic Analysis and Contribution to Airway Hyperresponsiveness Asthma is a complex disease characterized by airway hyperresponsiveness (AHR) and chronic airway inflammation. Environmental factors such as ambient particulate matter (PM), a major air pollutant, has been demonstrated in epidemiological studies to contribute to asthma exacerbation and increased asthma prevalence. OBJECTIVE: We investigated the genomic and pathophysiological effects of Baltimore PM (median diameter 1.78 µm) in a murine model of asthma to identify potential biomarkers. METHODS: A/J mice with ovalbumin (OVA) –induced AHR were exposed to PM (20 mg/kg, intratracheal), and both AHR and bronchoalveolar lavage (BAL) were assayed on days 1, 4, and 7 post exposure. Lung gene expression profiling (Affymetrix Mouse430_ 2.0) by PM (20 mg/kg, intratracheal) were assayed on OVA- and / or PM--challenged mice. RESULTS: Significant increases of airway responsiveness in OVA-treated mice were observed, indicating an asthmatic phenotype. Ambient PM exposure induced significant changes in AHR in both naive mice and OVA-induced asthmatic mice. In both naive and OVA challenged asthmatic mice, PM induced eosinophil and neutrophil infiltration into airways, elevated BAL protein content, and stimulated secretion of TH1 cytokines (IFN-g, IL-6, and TNF-a) and TH2 cytokines (IL-4, IL-5, and eotaxin) into BAL. Consistent with these results, PM induced expression of genes of innate immune response, chemotaxis and complementary system. CONCLUSION: These studies, consistent with epidemiological data, indicate that PM increases AHR and lung inflammation in naïve mice and exacerbates the asthma phenotype of increased AHR and gene expression pattern changes correlated with acute lung inflammation and airway damage. We used microarrays to detail the global programme of gene expression induced by rhPBEF treatment and VALI. Keywords: gene expression
2007-12-01 | GSE9465 | GEO