Breathing Polluted Air: Fetal Health At Risk

Breathing in air pollution during pregnancy can have a range of adverse effects on the fetus, including an increased risk of low birth weight, preterm birth, congenital abnormalities, and neonatal death. Research has also linked exposure to air pollution during pregnancy to fertility problems, miscarriage, and preeclampsia. Furthermore, air pollution can disrupt a baby's development, causing them to be born prematurely or with underdeveloped bodies and lungs. The specific effects depend on factors such as the duration and timing of exposure, as well as the type of pollutant. While it is challenging to completely avoid air pollution, pregnant individuals can take steps to reduce their exposure and protect their health and that of their unborn child.

Low birth weight

Exposure to air pollution during pregnancy has been linked to low birth weight in newborns. Low birth weight is defined as a newborn weighing less than 2500 grams. It is a significant risk factor for various health issues, developmental delays, and death after birth.

Several studies have found a correlation between exposure to air pollution and low birth weight. A 2013 analysis of 14 population-level studies found a higher prevalence of certain pollutants, such as nitrogen dioxide, correlated with a higher risk of low birth weight. Similarly, a study in Ahvaz, Iran, found a direct and significant relationship between exposure to particulate matter and sulfur dioxide and low birth weight. Another study in Guangdong, China, also found an association between exposure to particulate matter, sulfur dioxide, and ozone and low birth weight, especially during the first and third trimesters.

The mechanisms by which air pollution affects birth weight are not fully understood, but several factors are thought to be involved. Air pollution can cross the placenta,

Preterm birth

Breathing in air pollution can increase the risk of preterm birth, which is when a baby is born between 28 and 37 weeks of gestation. The risk of preterm birth is higher for people who live in polluted areas or are exposed to indoor air pollution, such as cigarette smoke.

A 2019 study found a correlation between air pollution and preterm labour, with the risk being highest during a subsequent pregnancy. The study, however, did not prove causation, and other factors may be responsible for the higher prevalence of preterm labour in polluted areas.

Several factors influence the specific effects of air pollution on pregnancy outcomes, including the timing and duration of exposure, as well as the type and amount of pollution.

Effects of Preterm Birth

Preventing Negative Effects of Air Pollution

While individuals typically cannot control pollution levels around their homes or workplaces, there are some strategies to reduce the harmful effects of polluted air:

• Evacuate to a safer area when air quality is very dangerous, such as during a wildfire.
• Install a carbon monoxide detector and a high-efficiency particulate air filter to reduce indoor air pollution.
• Avoid going outside during times of high pollution.
• Talk to a medical professional about other tips to reduce the overall risk of pregnancy complications related to air pollution.

Autism risk

Breathing in air pollution during pregnancy has been linked to an increased risk of autism in children. The evidence is particularly strong for exposure to fine particulate matter (PM2.5) during the pregnancy, especially in the third trimester. Ultrafine particles can cross the placenta, affecting the health of the placenta itself and disrupting fetal development.

Several studies have found a correlation between exposure to air pollution during pregnancy and autism spectrum disorder (ASD) in children. A 2023 cohort study from southern Sweden found that exposure to local, source-specific ambient air pollution during pregnancy was associated with an increased risk of childhood autism. The study looked at exposure to particulate matter (PM), specifically PM2.5, which is produced by residential wood burning and road traffic. The results suggested that locally produced PM2.5 from both residential heating and road traffic (tailpipe emissions and vehicle wear-and-tear) contributed to the increased risk of autism.

A 2020 systematic review and meta-analysis also found some evidence for a positive association between maternal exposure to PM2.5 and ASD. The review included 13 studies that investigated the association between ASD in children and PM2.5 exposure. The results showed a significant pooled odds ratio of 1.06 for prenatal exposure to PM2.5, indicating a 6% increase in the odds of ASD for every unit increase in PM2.5 exposure. The third trimester appeared to have the highest pooled odds ratio, suggesting that exposure during this period may be particularly critical.

Another study from Harvard T.H. Chan School of Public Health found that women exposed to high levels of PM2.5 during pregnancy, particularly during the third trimester, had up to twice the risk of having a child with autism compared to mothers living in areas with low particulate matter. The study population included offspring of participants living in all 50 states in the Nurses' Health Study II, a cohort of more than 116,000 female U.S. nurses. The researchers identified 245 children who were diagnosed with ASD and found a significant association between exposure to PM2.5 during pregnancy and autism, especially during the third trimester.

In addition to PM2.5, there is also some evidence of a positive association between maternal exposure to nitrogen dioxide (NO2) and ASD. The same 2020 systematic review and meta-analysis mentioned above found a significant pooled odds ratio of 1.02 for prenatal exposure to NO2, indicating a 2% increase in the odds of ASD for every unit increase in NO2 exposure. However, the evidence for this association is weaker compared to PM2.5.

While the exact mechanisms are not fully understood, several factors may contribute to the link between air pollution and autism. One potential mechanism is oxidative stress, which can damage cells and disrupt normal development. Exposure to air pollution has also been linked to inflammation, neurotoxicity, and endocrine disruption, which can all potentially impact brain development and increase the risk of neurodevelopmental disorders like autism.

Overall, the evidence suggests that breathing in air pollution during pregnancy, especially fine particulate matter (PM2.5), may increase the risk of autism in children. The third trimester appears to be a critical period for exposure, and the effects may be modulated by various factors such as genetics and other environmental influences. More research is needed to fully understand the underlying mechanisms and identify ways to mitigate the risks associated with air pollution exposure during pregnancy.

Asthma risk

Air pollution can have a detrimental impact on a developing fetus, increasing the risk of adverse health outcomes. One of the potential long-term consequences of exposure to air pollution during pregnancy is an increased risk of asthma in the child.

Air pollution has been linked to an increased risk of asthma, a serious and life-threatening chronic respiratory disease. Exposure to air pollution can worsen asthma symptoms and trigger asthma attacks. The estimated six million children in the United States with asthma are especially vulnerable to the effects of air pollution.

Research has found a connection between fetal exposure to air pollution and the development of asthma later in life. A study in Boston followed 376 women throughout their pregnancies and found that around 18% of the children developed asthma by the age of 3-4. The study also revealed that the timing of exposure played a role, with girls being more likely to develop asthma if exposed to air pollution later in the pregnancy, such as the third trimester. This timing remained constant for boys.

The mechanisms underlying the link between air pollution and asthma are still being explored. However, studies suggest that exposure to air pollutants can suppress genes involved in immune tolerance, leading to an increased risk of asthma. Additionally, air pollution may indirectly contribute to the development of asthma by causing low birth weight, early birth, or improper immune system development.

Particulate matter (PM), especially PM2.5, has been identified as a significant contributor to the risk of asthma. These tiny particles can penetrate deep into the lungs and even enter the bloodstream. Exposure to PM during pregnancy can have a detrimental impact on the developing fetus, increasing the risk of respiratory problems, including asthma, later in life.

Other air pollutants, such as ozone, nitrogen dioxide, and carbon monoxide, have also been linked to an increased risk of asthma. These pollutants can irritate the lungs and airways, triggering asthma symptoms and exacerbating the condition.

Overall, the evidence suggests that exposure to air pollution during pregnancy can increase the risk of asthma in the developing fetus, with potential long-term consequences for respiratory health.

Fertility problems

Breathing in air pollution can have a detrimental impact on fertility in both men and women. Air pollution can affect conception and birth rates, and the chemicals present in air pollution can interfere with hormones directly related to fertility.

Impact on male fertility

Several studies have found that air pollution has harmful effects on sperm quality in animals. A decrease in the daily production of spermatozoa and an increase in abnormal sperm shapes have been observed in mice and rats exposed to car exhaust, particularly from diesel vehicles. In humans, a small number of studies have been conducted, and these have found alterations in sperm parameters after exposure to air pollution, suggesting a decrease in sperm quality.

Impact on female fertility

A limited number of studies have been carried out on the impact of air pollution on female fertility, possibly due to the difficulties involved in such studies. However, the available research suggests that air pollution may have an impact on female reproductive parameters, particularly at the ovarian level. For example, a study on mice exposed to air pollution found a significant lengthening of their cycles and a decrease in the number of antral follicles compared to unexposed mice.

Impact on fertility treatments

Research on the impact of air pollution on in vitro fertilization (IVF) outcomes is limited, but the available studies suggest that air pollution may negatively affect IVF results. For example, a study on women undergoing their first IVF cycle found negative impacts of increased concentrations of nitrogen dioxide (NO2) on live births during all stages of the IVF cycle except the final stage. Another study on women exposed to high concentrations of large particulate matter during the follicular phase of the ovarian cycle found a two-fold increased rate of early miscarriages, regardless of whether the conception was natural or through IVF.

Mechanisms of action

Several mechanisms have been proposed to explain the impact of air pollution on fertility:

• Endocrine disruptor activity: Air pollutants, particularly polycyclic aromatic hydrocarbons (PAHs) and heavy metals contained in particulate matter, can act as endocrine disruptors. For example, diesel exhaust particles contain substances with estrogenic, antiestrogenic, and antiandrogenic activities that can affect gonadal steroidogenesis and gametogenesis.
• Generation of oxidative stress: Nitrogen dioxide (NO2), ground-level ozone (O3), and particulate matter (PM) can generate reactive oxygen species (ROS), which can cause alterations in DNA, proteins, and membrane lipids.
• Modifications of DNA: Air pollution can lead to the formation of DNA adducts, resulting in modifications in gene expression and/or the appearance of epigenetic mutations or modifications such as alterations in DNA methylation.
• Epigenetic modifications: Epigenetic changes, such as DNA methylation, can lead to abnormal gene expression and have been implicated in the effect of air pollution on carcinogenesis and respiratory failure.

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