Introduction

Women of reproductive age and during pregnancy – and subsequently newborns, infants, and young children – are particularly vulnerable to smog. Women’s exposure to NO₂ before pregnancy increases the risk of eczema in their children at preschool age [1]. Research indicates that air pollution in Europe accounts for over 1,200 deaths annually among individuals under 18 years of age [2]. Air pollution also constitutes a serious public health threat in Poland, estimated to cause approximately 50,000 premature deaths annually [3]. These data must be considered highly alarming. Globally, the World Health Organization (WHO) estimates that the combined effects of ambient (outdoor) and household air pollution lead to about 6.7 million premature deaths per year. Ambient outdoor air pollution alone was responsible for approximately 4.2 million deaths worldwide in 2019 [4]. Importantly, a significant fraction of this burden falls on children and pregnant women. In 2016, around 600,000 children under 15 years of age died due to air pollution-related illnesses, primarily acute lower respiratory infections [5]. WHO also reports that 93% of the world’s children live in areas where air quality fails to meet WHO guidelines [5]. Such global figures underscore that air pollution is not only a local problem but also a worldwide public health crisis. Literature emphasizes that the primary sources of pollution emissions in Poland originate from road transport and combustion processes in municipal and household sources. Another significant source of exposure, particularly for children, is environmental tobacco smoke (ETS) in indoor environments. Children’s exposure to secondhand tobacco smoke remains alarmingly common. Globally, over 40% of children are regularly exposed to tobacco smoke at home; in Poland this figure exceeds 30%. The health consequences of such exposure overlap with those of ambient air pollution, contributing to respiratory infections, developmental issues, and other diseases. ETS exposure can thus act as a confounding factor when assessing the impacts of outdoor air pollution on child health, and it is crucial for studies to account for children’s tobacco smoke exposure alongside environmental pollution [6].

One of the key parameters of air pollution is parti­culate matter (PM), a complex mixture of solid particles and liquid droplets that can adsorb carcinogenic compounds such as benzo[a]pyrene (BaP; classified as a group 1 carcinogen), as well as toxic metals (lead, cadmium, nickel) and metalloids (e.g., arsenic). PM₁₀ particles have a diameter no greater than 10 µm, PM_2.5 particles no greater than 2.5 µm, and PM_0.1 particles less than 0.1 µm. Particles smaller than 0.1 µm are considered the most hazardous because no natural barriers prevent their entry into the body [7].

PM acts as a carrier for many substances, which, even as PM_2.5, easily enter the bloodstream [8]. Young children, due to shorter and narrower respiratory tracts, often breathe through their mouths, creating additio­nal difficulties for their immature detoxification systems and insufficient nasal filtration. Additionally, children tend to spend more time outdoors, engaging in significantly higher levels of physical activity than adults. Per kilogram of body weight, a child has a higher minute ventilation than an adult, and their respiratory tracts are closer to the ground (due to height), making them more susceptible to roadside pollution [9]. In the case of BaP, Poland records significant exceedances of standards in many zones – the highest among Euro­pean countries [10]. In 2023, in 46 air quality measurement zones, BaP standards were exceeded 21 times.

In recent years, the urban population of Poland has been exposed to elevated BaP concentrations, exceeding norms by as much as 70–100%. Figure 1 illustrates the percentage of the Polish urban population exposed to EU norm exceedances for BaP and other major air pollutants. Figure 2 illustrates Poland as the country with the highest exceedance of BaP pollution levels.

Methods

This article is based on a comprehensive literature review of the impacts of air pollution on the health of children and women of reproductive age. The lite­rature search was conducted using scientific data­bases (PubMed, Web of Science, and Google Scholar) for articles published primarily in the last 10 years (through 2025) and key authoritative reports by organizations such as the World Health Organization (WHO) and the European Environment Agency. Search terms included combinations of keywords such as “air pollution,” “child health,” “pregnancy,” “prenatal exposure,” “particulate matter,” “ETS” and specific outcomes (e.g., “asthma,” “birth weight,” “neurodevelopment,” and “preeclampsia”). Studies were included if they examined the health impacts of outdoor air pollutants (e.g., PM_2.5, PM₁₀, NO₂, O₃) or important indoor pollutants (such as tobacco smoke) in pregnant women and in fetuses, infants, or children. Both epidemiological studies (cohort, case-control, cross-sectional) and experimental studies were considered, as well as systematic reviews, meta-analyses, and selected high-impact case studies. No formal quantitative meta-analysis was performed in this narrative review; instead, findings from the lite­rature were synthesized qualitatively. Priority was given to recent studies and those covering the populations of interest (pediatric and perinatal health) and to data from global health authorities. The evidence gathered was organized thematically by organ system or health outcome (reproductive outcomes, respiratory system, cardiovascular system, nervous system, metabolic effects, and cancer outcomes). In the following sections, the findings are summarized according to these themes, and potential biological mechanisms that may explain the observed health effects are discussed. All relevant sources have been cited, and a full list of references is provided at the end of this article.

Biological mechanisms of pollution-induced health effects

Air pollutants can initiate a cascade of biological damage through multiple interrelated mechanisms. A primary pathway is oxidative stress: inhaled pollutants such as PM_2.5 and ozone generate reactive oxygen species (ROS) that overwhelm the body’s antioxidant defenses. This oxidative stress damages cells and tissues, and in turn triggers inflammatory responses [11].

Chronic inflammation driven by pollutant exposure has been documented, with PM and traffic-related pollutants promoting the release of pro-inflammatory cytokines in the lungs and systemically. Such persistent inflammation can impair normal organ development in children and exacerbate underlying conditions [12]. Another mechanism involves disruptions of the microbiome. Components of air pollution, including toxic heavy metals adhering to particulates, can alter the composition of the gut microbiota. Pollutant-induced microbiome dysbiosis may contribute to immune dysregulation and metabolic disturbances in children, and available studies suggest that exposure to heavy metals present in air pollution is associated with alterations in gut microbial communities that may increase the risk of metabolic and autoimmune diseases [13]. Perhaps the most far-reaching effects of early-life pollution exposure are mediated by epigenetic changes. Research shows that prenatal exposure to pollutants such as fine parti­culates (PM_2.5), polycyclic aromatic hydrocarbons (from combustion), and heavy metals can lead to alterations in DNA methylation patterns in the fetus and newborn [14]. These epigenetic modifications – occurring without changes to the DNA sequence – can reprogram gene expression in ways that persist into later life, thereby increasing susceptibility to various disorders. For instance, maternal exposure to air pollution has been associated with DNA methylation changes in placental and fetal tissue, potentially affecting genes involved in growth and immune regulation [15]. Such epigenetic imbalances are thought to be one route by which early pollution exposure elevates the risk of diseases in children. Notably, similar epigenetic effects are seen with prenatal tobacco smoke exposure: studies have found that parental smoking can lead to DNA hypomethy­lation and other changes in the child’s genome that are associated with higher cancer risk later in life [16].

Impact of air pollution on reproductive health and prenatal development

Elevated concentrations of PM in pregnant women may adversely affect placental microcirculation, contributing to oxidative stress and chronic inflammation in both the mother and developing fetus. Studies confirm an association between PM_2.5 exposure and a significantly higher risk of low birth weight. Meta-analyses indicate that even a slight annual increase in PM_2.5 concentration (by 1 µg/m³) can decrease average birth weight by several grams [17]. These mechanisms are also associated with implantation disorders, premature placental detachment, and restricted fetal growth, increasing the risk of miscarriages and premature births [18].

Air pollution negatively affects fertility in both women and men. Chronic exposure to high levels of PM and toxic substances contributes to poorer semen quality, reduced sperm count, and hormonal dysfunction in ovaries, hindering conception and reducing the effectiveness of infertility treatments using assisted reproduction [19].
An analysis involving nearly one million births in 30 sub-Saharan African countries showed that a 10 µg/m³ annual average increase in PM_2.5 concentration was associated with a 9% increase in infant mortality, irrespective of family economic status. It is estimated that over 20% of infant deaths in this region are related to air pollution exposure [20]. It is important to emphasize that secondhand exposure to tobacco smoke (ETS) during pregnancy is also associated with a marked increase in the risk of obstetric complications and adverse fetal outcomes. In pregnant non-smoking women living with a smoker, preterm delivery is observed significantly more often – a meta-analysis of cohort studies showed an approxima­tely 20% increase in the risk of delivery before 37 weeks of gestation in the case of ETS exposure [21]. Similarly, to­xins from tobacco smoke (including nicotine and carbon monoxide, which cross the placenta) impair fetal growth, increasing the incidence of intrauterine growth restriction and low birth weight in newborns [22].

Respiratory system

Studies evaluating the impact of particulate pollutants (PM₁₀ and PM_2.5) on children’s health in Warsaw indicated significant health risks. Annually, approximately 5,000 asthma exacerbations and over 200 respiratory-related hospitalizations in children are directly associated with PM exposure [23]. A retrospective study in Kraków (2014–2015) identified a significant asso­ciation between air pollution and the incidence of subglottic laryngitis in children [24]. Short-term exposure to PM, NO₂, SO₂, O₃, and CO also increases the risk of respiratory infections. Areas in Poland with the highest PM concentrations have approximately 10% more upper respiratory tract infections compared to cleaner regions. In a study conducted during the heating season of 2018/2019, 1,475 children aged 3–12 years were moni­tored, with parents recording daily symptoms of upper respiratory tract infections (runny nose, cough, sneezing) using a mobile application linked to an air pollution monitoring system. Analysis showed that in areas with the highest particulate concentrations, symptoms such as runny nose, cough, and sneezing were approximately 10% more frequent than in cities with the lowest concentrations. Furthermore, higher concentrations of PM_2.5 were associated with cognitive dysfunction in up to 35% of children living in highly polluted environments [25].

Children are particularly vulnerable to respiratory infections caused by pollution both postnatally and due to prenatal exposure. PM can cross the placenta, disrupting lung development through oxidative stress and epigenetic changes [26]. These effects are more pronounced in premature infants, causing lasting changes in the respiratory system and increased risk of infections in early childhood [27]. Air pollutants, including PM, nitrogen oxides (NO, NO₂), ozone (O₃), sulfur dioxide (SO₂), and carbon monoxide (CO), induce significant oxidative stress in the respiratory system, damaging cells and exacerbating inflammatory responses, thereby increasing susceptibility to respiratory infections [28]. PM_2.5 promotes the production of pro-inflammatory cytokines and reduces antiviral immunity by decreasing macrophage mobility and mucociliary clearance [29]. Prenatal exposure to high concentrations of PM_2.5 increases the risk of lower respiratory tract infections during the first year of life. Similar effects are caused by other pollutants, such as PM₁₀ and SO₂, which increase pneumonia incidence [30]. Air pollution also negatively affects oral health. In children with asthma, exposure to PM_2.5 can trigger an inflammatory response in the oral cavity, as evidenced by increased interleukin-6 levels in saliva, which correlates with worsened asthma symptoms [31]. Prematurely born children, even without considering air pollution exposure, exhibit numerous abnormalities in oral morphology, such as high palate arching, reduced dental arch dimensions, delayed eruption of primary teeth, moderate to severe occlusal and dental anomalies (crossbite, distal occlusion, crowding), and more frequent enamel mineralization disorders such as hypomineralization and hypoplasia [32]. Additionally, children exposed to secondhand smoke have a significantly poorer respiratory health status. Studies have shown that contact with ETS results in more frequent respiratory tract infections (bronchitis and pneumonia) and a higher tendency toward recurrent otitis media [33]. Moreover, these children are more likely to develop asthma – meta-analyses confirm an approximately 20–30% increase in the risk of asthma and wheezing in children exposed to tobacco smoke at home [34]. Chronic exposure to ETS also adversely affects lung development and function – in children living in smoke-polluted environments, reductions in spirometric parameters (FVC, FEV₁) and a slower increase in lung capacity have been observed [35].

Cardiovascular system

Air pollution exposure has significant effects on the cardiovascular system of both children and pregnant women. In children, studies have linked chronic exposure to polluted air with elevated blood pressure and early signs of vascular dysfunction. A meta-analysis of 14 studies from various countries found that childhood exposure to high levels of air pollutants increases the likelihood of high blood pressure in children and adolescents, and also raises the risk of hypertension in adulthood [36]. Even short-term spikes in particulate levels can acutely raise blood pressure in youth. Such changes in blood pressure during early life are concerning, as high blood pressure in childhood is a risk factor for cardiovascular disease later on. Moreover, emerging evidence indicates that long-term pollution exposure contributes to subclinical atherosclerosis in young individuals. Signs of pre-symptomatic stiffening of the arteries have been observed in children with daily exposure to heavy traffic emissions [37]. For example, one cohort study in Southern California found that greater childhood exposure to traffic-related air pollutants was associated with a significantly increased progression of carotid intima-media thickness (an early indicator of atherosclerosis) from childhood into young adulthood. This suggests that polluted air can begin to induce vascular changes even in the first decades of life, potentially setting the stage for earlier onset of cardiovascular disease [38].

For pregnant women, air pollution poses risks to cardiovascular health both during pregnancy and beyond. Maternal exposure to ambient air pollutants has been associated with an increased risk of hypertensive disorders of pregnancy, including gestational hypertension and preeclampsia [39]. A systematic review and meta-analysis demonstrated that each 10 µg/m³ increase in long-term PM_2.5 exposure during pregnancy is associated with roughly a 32% higher odds of developing preeclampsia [40]. Pollution-related oxidative stress and endothelial dysfunction are thought to contri­bute to these pregnancy complications. Women who are exposed to high levels of traffic-related air pollution have shown higher blood pressure during pregnancy and a greater likelihood of preeclampsia onset. Such conditions not only endanger the mother’s health (e.g., risk of stroke, organ damage during pregnancy) but also can impair uteroplacental blood flow, thereby affecting fetal growth and health [41].

In addition, evidence suggests that exposure to air pollution during pregnancy can have long-term effects on a child’s cardiovascular system. Some studies report that infants born to mothers exposed to higher pollutant levels show differences in vascular function and may be more likely to develop elevated blood pressure in early childhood, indicating a link between maternal air quality and the child’s future cardiovascular risk [42].

Population-based and cohort studies confirm that regular exposure to ETS (4–7 days per week or ≥ 2 hours per day) is associated with an 18–27% higher risk of hypertensive disorders of pregnancy compared with non-exposed women [43]. Children exposed to ETS prenatally and postnatally have higher blood pressure and an increased risk of developing hypertension and carotid intima-media thickening, which is an early marker of atherosclerosis [44]. It has been demonstrated that childhood exposure to ETS leads to persistent changes in vascular function, lipid abnormalities, and chronic low-grade inflammation, thereby increasing the risk of cardiovascular disease in adulthood [45].

Nervous system

The impact of air pollution on the nervous system of children and adolescents is highly concerning. Exposure to PM, especially PM_2.5 , may increase the risk of developing pathologies typical for Alzheimer’s disease in children and adolescents with genetic predispositions. Proposed mechanisms include inducing oxidative stress, producing inflammatory cytokines, and damaging the blood–brain barrier [46]. Additionally, correlations have been observed between chronic air pollution exposure and mood disorders, behavioral problems, and concentration difficulties [47]. Prolonged exposure to high concentrations of PM and traffic emissions, both prenatally and during early childhood, leads to negative health outcomes affecting the nervous system. Cognitive impairment, delayed speech development, learning difficulties, and deficits in attention, working memory, and executive functions have been observed. Studies indicate a potential association between air pollution exposure and autism spectrum disorders and attention-deficit/hyperactivity disorder (ADHD), possibly through neuroinflammatory mechanisms and oxidative stress resulting from pollutant penetration across the blood–brain barrier. Analyses of rural populations have shown that exposure to air pollutants (NO₂, O₃, SO₂, PM₁₀) is associated with higher frequencies of behavioral disorders, anxiety, ADHD, and eating disorders among children living in rural areas [48].

A growing body of evidence indicates that passive exposure to tobacco smoke in early life adversely affects the development of the nervous system in children. Toxic components of tobacco smoke (including nicotine, carbon monoxide, and heavy metals) disrupt neurogenesis and may lead to lasting alterations in the structure and function of the developing brain [49]. Population-based studies have demonstrated an association between ETS exposure and a higher prevalence of neurodevelopmental disorders in children. For example, a meta-analysis of 54 studies estimated that, among children whose mothers were exposed to tobacco smoke during pregnancy, the risk of developing ADHD and specific learning difficulties is significantly higher than among non-exposed peers [50].

Summary

The analyzed data clearly indicate that children are particularly vulnerable to the adverse health effects of air pollution and ETS exposure, both prenatally and during the early years of life. These effects cover a wide spectrum, from developmental and growth disorders to increased risks of infections and neuropsychological diseases. Until now, studies on the mental health impact of air pollution in children have focused mainly on urban environments; however, analyses of rural populations have shown that exposure to air pollution (NO₂, O₃, SO₂, PM₁₀) is also associated with higher incidences of behavioral, anxiety, ADHD, and eating disorders in children living in rural areas. It should be strongly emphasized that passive exposure to tobacco smoke represents a significant health threat to pregnant women and children. In this population, ETS increases the risk of obstetric complications such as gestational hypertension, preeclampsia, and low birth weight in newborns. In children, it contributes to the development of respiratory diseases, neurocognitive disorders, hypertension, and cancer. Studies clearly confirm that ETS exposure – even in the absence of active smoking – can lead to serious, long-term health consequences.

The suggestions emerging from the presented lite­rature review strongly confirm the need to implement effective preventive measures at both the systemic level (such as improving air quality and controlling emissions) and the individual level (including health education and reducing children’s exposure to pollutants). From an ethi­cal standpoint, every child has the right to proper, harmonious physical and mental development.

Conclusions

Protecting the health of children and pregnant women from air pollution should be a top priority in public health policy, especially in regions with poor air quality. The evidence compiled in this review makes it clear that air pollution has multi-organ adverse effects on these vulnerable populations, contributing to fetal growth problems, childhood respiratory and cardiovascular conditions, and neurodevelopmental disorders. Given these findings, there is an urgent need for concrete and operational measures to mitigate air pollution exposure. Stricter air quality standards and emissions controls should be implemented to reduce levels of PM_2.5, NO_x, and other harmful pollutants, with a focus on high-risk areas and periods (e.g., urban centers and heating seasons). Additionally, targeted interventions such as expanding green zones, promoting clean household fuels, and enforcing smoking bans in homes and cars can help limit children’s and pregnant women’s contact with pollutants. Healthcare providers and policymakers should also invest in preventive strategies at the individual level: educating parents and communities about the health risks of air pollution and ETS, advising pregnant women and families on exposure-reducing behaviors, for example, using air filtration indoors on high pollution days, or avoiding outdoor exercise near heavy traffic.

Disclosures

1. Institutional review board statement: Not applicable.

2. Assistance with the article: None.

3. Financial support and sponsorship: None.

4. Conflicts of interest: None.

References