There is suggestive evidence linking PM exposure to central nervous system, developmental and reproductive health effects.
4.6.1
Central nervous system effects
There is limited evidence that exposure to high levels of PM air pollution can be detrimental to the central nervous system (CNS) and perhaps contribute to neurodevelopmental and neurodegenerative diseases such as, autism spectrum disorders, Alzheimer’s disease and Parkinson’s disease. In Canada, the amount of manganese in ambient PM has been we akly associated with the number of diagnoses for Parkinson’s disease, which is consistent with the theory that exposure to manganese adds to the loss of neurons during aging (Finkelstein and Jerrett 2007). Residential proximity to traffic and, gestational and early life exposure to traffic-related air pollution and diesel exhaust emissions have been associated with autism spectrum disorders (Costa et al. 2014). Autopsy brain tissue from individuals who lived in areas with high air pollution levels is suggestive of air pollution exposure contributing to enhanced CNS inflammation and the pathological signs of Alzheimer’s disease (Calderon-Garciduenas et al. 2004). Magnetic resonance imaging of the brains of children exposed to high ambient air pollution in Mexico City demonstrated an increase in brain lesions in these children (Calderon-Garciduenas et al. 2008). Children in Mexico City have signs of both neuro- and systemic inflammation (Calderon-Garciduenas et al. 2007). Young and old individuals appear to be particularly susceptible to air pollution-induced neurotoxicity (Costa et al. 2014). Closure of a coal-fired power plant in China was associated with a reduction in exposure to PAHs and improvements in neurological and cognitive development in children (Tang et al. 2014). The primary mechanisms of air pollution neurotoxicity appear to be related to oxidative stress and inflammation. The brain is vulnerable to both of these processes (MohanKumar et al. 2008). Animals exposed to concentrated PM have enhanced inflammation in the brain and neurop athology (Campbell et al. 2005, Kleinman et al. 2008, Block and Calderon-Garciduenas 2009). Dogs from an urban area exposed to high levels of air pollution demonstrated accelerated Alzheimer’s -type
58 pathology and CNS inflammation compared to dogs from a cleaner air location (Calderón- Garcidueñas et al. 2003). The PM-associated metals nickel and vanadium were detected in the brains of the dogs from the polluted city. Initial evidence from animal studies suggests that exposure to diesel engine exhaust particulates may increase CNS inflammation and cause developmental neurotoxicity (Levesque et al. 2011, Costa et al. 2014).
Systemic inflammation can cause CNS inflammation and neurotoxicity and, is implicated in neurodegenerative disease (Block and Calderon-Garciduenas 2009). Thus it may be that the neurological effects of PM air pollution are a result of systemic inflammation. It is also possible that particles in the systemic circulation translocate into the CNS (Oberdorster et al. 2004, Peters et al. 2006, Calderon-Garciduenas et al. 2008). The evidence in humans, albeit limited, suggests that exposure to PM may adversely affect the CNS.
4.6.2
Developmental and reproductive effects
Exposure to air pollution (and specifically PM) during pregnancy appears to retard foetal growth, as evidenced by associations between exposure and low term birth weights, albeit with considerable variability in results from different regions (Wilhelm and Ritz 2005, Heinrich and Slama 2007, Millman et al. 2008, Parker et al. 2011, Dadvand et al. 2013). Exposure to PM2.5 from traffic has been associated with low term birth weights in Los Angeles (Wilhelm et al. 2012). Exposure to PM during pregnancy has also been associated with an increased risk of pre -term birth (Wilhelm and Ritz 2005, Rappazzo et al. 2014). It is not clear whether PM directly affects the foetus or whether effects on the health of the mother are responsible for these adverse birth outcomes. However, the presence of PAHs attached to DNA in umbilical cord blood indicates that air pollutants can transfer to the foetus (Tang et al. 2006). High PAH-DNA adducts in cord blood have been associated with decreased body weight in the first few years of childhood (Tang et al. 2006). Pre-natal exposure to PAHs in air has been associated with morphological changes related to cognitive deficits and behavioural problems in the brains of children aged 7-9 years (Peterson et al 2015).
Lung development continues well into childhood and postnatal exposure to PM2.5 is associated with impaired lung growth and decreased lung function later in life (Gauderman et al. 2004, Schuepp and Sly 2012). Children who moved to locations with higher ambient PM have demonstrated a slowing in lung function development, whereas children who have moved to areas with cleaner air have demonstrated an increase in lung function development (Avol et al. 2001).
Pre- and post-natal exposure to diesel exhaust particulates in animals has been associated with a variety of developmental and reproductive effects including retarded growth of offspring, abnormal development of the female and male reproductive systems, altered sperm development and, increased mutation rates in male germline cells (Ema et al. 2013). It has been suggested that inhalation of PM could result in heritable mutations by causing mutations in sperm (Samet et al. 2004), however there is no human evidence for this. There is the suggestion that exposure to air pollution may be associated with a reduction in sperm quality (Selevan et al. 2000) and this could reduce fertility rates. This effect may be related to the oxidative stress effects of PM as increased oxidative stress is associated with decreases in sperm motility (Ruckerl et al. 2011).
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