Dataset Information

Differential impacts of particulate air pollution exposure on early and late stages of spermatogenesis.

ABSTRACT:

Background

Despite increasing evidence that particulate air pollution has adverse effects on human semen quality, few studies examine the impact of air pollution on clinically relevant thresholds used to diagnose male fertility problems. Furthermore, exposure is often assessed using average air pollution levels in a geographic area rather than individualized estimates. Finally, physiologically-informed exposure windows are inconsistent.

Objectives

We sought to test the hypothesis that airborne particulate exposures during early-phase spermatogenesis will have a differential impact on spermatogenic formation compared to late-phase exposures, using an individualized model of exposure to particulate matter ≤ 2.5 µm and ≤ 10 µm (PM_2.5 and PM₁₀, respectively).

Methods

From an original cohort of 183 couples, we conducted a retrospective analysis of 130 healthy males seeking to become parents, using spermatogenesis-relevant exposure windows of 77-34 days and 37-0 days prior to semen collection to encompass sperm development stages of mitosis/meiosis and spermiogenesis, respectively. Individualized residential exposure to PM_2.5 and PM₁₀ was estimated by selecting multiple air pollution sensors within the same geographic air basin as participants and employing inverse distance weighting to calculate mean daily exposure levels. We used multiple logistic regression to assess the association between pollution, temperature, and dichotomized World Health Organization semen parameters.

Results

During the early phase of spermatogenesis, air pollution exposure is associated with 1.52 (95% CI: 1.04-2.32) times greater odds of < 30% normal heads per 1-unit increase in IQR for PM_2.5. In the late phase of spermatogenesis, air pollution exposure is associated with 0.35 (95% CI: 0.10-0.74) times greater odds of semen concentration < 15 million/mL per 1-unit increase in IQR for PM_2.5, and 0.28 (95% CI: 0.07-0.72) for PM₁₀.

Conclusion

Particulate exposure has a differential and more deleterious impact on sperm during early-phase spermatogenesis than late-phase.

SUBMITTER: Henry TD

PROVIDER: S-EPMC8383784 | biostudies-literature | 2021 Sep

REPOSITORIES: biostudies-literature

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Publications

Differential impacts of particulate air pollution exposure on early and late stages of spermatogenesis.

Henry Trenton D TD Porucznik Christina A CA Honda Trenton J TJ VanDerslice James A JA Blackburn Brenna E BE Cox Kyley J KJ Carrell Douglas T DT

Ecotoxicology and environmental safety 20210611

<h4>Background</h4>Despite increasing evidence that particulate air pollution has adverse effects on human semen quality, few studies examine the impact of air pollution on clinically relevant thresholds used to diagnose male fertility problems. Furthermore, exposure is often assessed using average air pollution levels in a geographic area rather than individualized estimates. Finally, physiologically-informed exposure windows are inconsistent.<h4>Objectives</h4>We sought to test the hypothesis ...[more]

PMID: 34126304

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Project description:BackgroundChronic exposure to particulate air pollution may accelerate cognitive decline in older adults, although data on this association are limited. Our objective was to examine long-term exposure to particulate matter (PM) air pollution, both coarse ([PM 2.5-10 μm in diameter [PM(2.5-10)]) and fine (PM <2.5 μm in diameter [PM(2.5)]), in relation to cognitive decline.MethodsThe study population comprised the Nurses' Health Study Cognitive Cohort, which included 19,409 US women aged 70 to 81 years. We used geographic information system-based spatiotemporal smoothing models to estimate recent (1 month) and long-term (7-14 years) exposures to PM(2.5-10), and PM(2.5) preceding baseline cognitive testing (1995-2001) of participants residing in the contiguous United States. We used generalized estimating equation regression to estimate differences in the rate of cognitive decline across levels of PM(2.5-10) and PM(2.5) exposures. The main outcome measure was cognition, via validated telephone assessments, administered 3 times at approximately 2-year intervals, including tests of general cognition, verbal memory, category fluency, working memory, and attention.ResultsHigher levels of long-term exposure to both PM(2.5-10) and PM(2.5) were associated with significantly faster cognitive decline. Two-year decline on a global score was 0.020 (95% CI, -0.032 to -0.008) standard units worse per 10 μg/m(3) increment in PM(2.5-10) exposure and 0.018 (95% CI, -0.035 to -0.002) units worse per 10 μg/m(3) increment in PM(2.5) exposure. These differences in cognitive trajectory were similar to those between women in our cohort who were approximately 2 years apart in age, indicating that the effect of a 10-μg/m(3) increment in long-term PM exposure is cognitively equivalent to aging by approximately 2 years.ConclusionLong-term exposure to PM(2.5-10) and PM(2.5) at levels typically experienced by many individuals in the United States is associated with significantly worse cognitive decline in older women.

Project description:BackgroundAir pollution nowadays has seriously threatened the health of the Chinese population, especially in the vulnerable groups of fetuses, infants and toddlers. In particular, the effects of air pollution on children's neurobehavioral development have attracted widespread attention. Moreover, the early detection of a sensitive period is very important for the precise intervention of the disease. However, such studies focusing on hyperactive behaviors and susceptible window identification are currently lacking in China.ObjectivesThe study aims to explore the correlation between air pollution exposure and hyperactive behaviors during the early life stage and attempt to identify whether a susceptible exposure window exists that is crucial for further precise intervention.MethodsBased on the Longhua Child Cohort Study, we collected the basic information and hyperactivity index of 26,052 children using a questionnaire conducted from 2015 to 2017, and the Conners' Parent Rating Scale-revised (CPRS-48) was used to assess hyperactive behaviors. Moreover, the data of air pollution concentration (PM10, PM2.5, NO2, CO, O3 and SO2) were collected from the monitoring station between 2011 to 2017, and a land-use random forest model was used to evaluate the exposure level of each subject. Furthermore, Distributed lag non-linear models (DLNMs) were applied for statistic analysis.ResultsThe risk of child hyperactivity was found to be positively associated with early life exposure to PM10, PM2.5 and NO2. In particular, for an increase of per 10 µg/m3 in PM10, PM2.5 and NO2 exposure concentration during early life, the risk of child hyperactivity increased significantly during the seventh month of pregnancy to the fourth month after birth, with the strongest association in the ninth month of pregnancy (PM10: OR = 1.043, 95% CI: 1.016-1.071; PM2.5: OR = 1.062, 95% CI: 1.024-1.102; NO2: OR = 1.043, 95% CI: 1.016-1.071). However, no significant associations among early life exposure to CO, O3 and SO2 and child hyperactive behaviors were observed.ConclusionsEarly life exposure to PM10, PM2.5 and NO2 is associated with an increased risk of child ADHD-like behaviors at the age around 3 years, and the late-prenatal and early postnatal periods might be the susceptible exposure windows.

Dataset Information

Differential impacts of particulate air pollution exposure on early and late stages of spermatogenesis.

Background

Objectives

Methods

Results

Conclusion

Publications

Differential impacts of particulate air pollution exposure on early and late stages of spermatogenesis.

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