CCCEH Research: Krakow, Poland

Krakow is a highly industrialized city with accordingly high levels of combustion-generated pollutants (PAHs, PM2.5) from extensive coal burning (industry, home heating) and vehicular traffic, as well as high rates of infant mortality, low birth weight, and cancer. Begun in 2000, the study has enrolled 505 pregnant women and, once born, their infants. Families live in one of two selected areas of Krakow—the Srodmiescie, Old Podgorze area which has relatively high air pollution levels and the Krowodrza, Nowa Huta, New Podgorze area with lower air pollution levels. This cohort is exposed to very high levels of air pollution—a level that is comparable to several other European cities. Results of the study therefore apply to other similar populations.

Methods

CCCEH investigators collaborate with a research team from Jagiellonian University in Krakow to examine the vulnerability of the fetus and infant to common environmental pollutants from fuel combustion (PAHs, PM2.5), secondhand smoke (ETS), mercury, and lead. Similar to the Center’s other studies, exposure of the Polish cohort is measured by individual air monitoring of environmental pollutants in the air women breathe during pregnancy, and the collection of biological samples to study various “biomarkers”—a biochemical compound indicating susceptibility and exposure to, as well as damage from, environmental pollutants. Currently, children in the study are being followed from birth through age 9 years.

Policy

This study is providing much needed information on the serious health effects to children exposed to chronic high levels of air pollution in Krakow. CCCEH shares its scientific findings with government authorities and public interest groups that are working to improve Krakow’s environmental health by advocating for wider use of cleaner fuels and clean air technologies.

Research Findings

Study results indicate that pregnant women have substantial prenatal exposure to the pollutants under study. Findings indicate that birth outcomes, children’s early neurodevelopment, and respiratory health are adversely affected by prenatal exposures to these environmental pollutants:

Prenatal Environmental Exposures

  • Children in the study have substantial and variable prenatal exposure to the air pollutants of concern and birth outcomes, neurodevelopment at 12 months, and asthma risk at ages 6 and 12 months are adversely affected by prenatal exposures (Jedrychowski, et al., 2003).
  • Pregnant women in Krakow have about 10-fold higher PAH (byproduct of fuel combustion from home heating, industry and vehicular traffic) exposure as measured in the air they are breathing, compared to pregnant women participating in the equivalent study in New York City (Adibi, et al., 2003).
  • Pregnant women’s exposure to PAH is significantly higher during the winter months and indoor concentration is a better predictor of short-term exposure, while outdoor concentration is more useful as a long-term predictor (Choi, et al., 2008). High prenatal exposure to airborne PAH and PM2.5 led to a reduction in birth weight, length and head circumference. Previous studies have shown that reduced birth size can adversely affect children’s learning ability and increase their risk of health problems (Jedrychowski, et al., 2003).
  • Approximately 40 percent of pregnant women reported exposure to environmental tobacco smoke (ETS) at home or work. Cotinine levels measured in newborns’ plasma were significantly higher than in mothers, indicating that the fetus is less able to detoxify this substance (Jedrychowski, et al., 2007).

Birth Outcomes

  • Pregnant women’s exposure to PAHs is significantly higher in the heating season and high prenatal exposure to airborne PAHs and PM2.5 led to a reduction in birth weight, length, and head circumference (Choi, et al., 2006). Previous studies have shown that reduced birth size can adversely affect children’s learning ability and increase their risk of health problems (Jedrychowski, et al., 2003).

Developmental Delay

  • Prenatal ETS exposure was inversely related to one and two year mental and motor development. This means that the higher the exposure, the lower the developmental test score (Jedrychowski, et al., 2006).
  • Significant adverse effects of prenatal mercury exposure were found on one year mental and motor development and a suggested effect on two year motor development (Jedrychowski, et al., 2005).
  • Prenatal exposure to airborne PAH was associated with adverse effects on children’s cognitive development at age 5, which parallels findings from similar studies performed in New York City (Edwards, et al., submitted 2009).
  • There is evidence to suggest that male children are more susceptible than female children to the adverse effects of very low-level prenatal lead exposure on cognitive function at age 3 (Jedrychowski, et al., 2009).

Respiratory Symptoms

Prenatal exposure to PAHs and second-hand smoke are increasing children’s respiratory symptoms and likelihood of developing asthma.

  • In the first year of life, research results indicate that prenatal PAH exposure was associated with the occurrence of various respiratory symptoms such as barking cough, wheezing, cough irrespective of respiratory infections, and cough without cold. PAH exposure also had an impact on the duration of respiratory symptoms (Jedrychowski, et al., 2007).
  • The effect of PAH on the risk of such symptoms as runny nose or cough was increased by postnatal secondhand smoke (ETS) exposure. A similar analysis performed for the duration of respiratory symptoms confirmed a significant PAH/ETS interaction for runny or stuffy nose, cough, difficulty breathing, and sore throat (Jedrychowski, et al., 2007).
  • Higher levels of prenatal exposure to fine particles (PM2.5) was associated with increased wheezing in children and more days with difficult breathing in the first two years of life (Jedrychowski, et al., 2008).

Increased Cancer Risk

  • Pregnant women in this study have about a 30-fold higher level of exposure to PAHs as measured in the air they are breathing compared to women in the Center’s New York City study, and genetic damage from PAHs measured in maternal and newborn (umbilical cord) blood was higher in Krakow than in NYC. Despite the fact that the placenta reduces the dose of PAHs by 10-fold or more, genetic damage in newborns in both cohorts was similar to that in their mothers. This indicates that newborns showed increased susceptibility to procarcinogenic damage — a result of great concern because babies have a much longer life course tan adults over which cancer can develop as a result of such early damage (Perera, et al., 2004).

Nutrition and Genes

There is variation among the children participating in our study in response to the same level of exposure. This indicates differences in susceptibility due to genetic or nutritional factors. The following studies try to understand the effects of these modifying factors on:

Birth Outcomes:
  • Maternal concentration of lipid-soluble plasma micronutrients were positively associated with birth weight and head circumference indicating that these micronutrients may have a direct effect on these pregnancy outcomes (Masters, et al., 2007).
  • Findings have shown benefits of fish consumption during pregnancy. Babies born to women who reported high fish intake during their third trimester of pregnancy did not have reduced birth size that our research previously associated with prenatal exposure to fine air particulate matter (Jedrychowski, et al., 2007).
Cancer:
  • Results from a study on the association between antioxidants and PAH-DNA adducts (covalent bonds between DNA and carcinogenic compound) suggest a protective effect of these micronutrients regarding DNA damage, which may decrease the potential cancer risk associated with prenatal exposure to PAH (Kelvin, et al., 2009).
Neurodevelopment:
  • A recent study finds evidence that genotypes may influence the effects of PAHs on neurodevelopmental outcomes, rendering some populations more vulnerable to these pollutants than others (Wang, et al., 2009).