Moniek Zuurbier

Improving health through policies that promote active travel: A review of evidence to support integrated health impact assessment

BACKGROUND Substantial policy changes to control obesity, limit chronic disease, and reduce air pollution emissions, including greenhouse gasses, have been recommended. Transportation and planning policies that promote active travel by walking and cycling can contribute to these goals, potentially yielding further co-benefits. Little is known, however, about the interconnections among effects of policies considered, including potential unintended consequences. OBJECTIVES AND METHODS We review available literature regarding health impacts from policies that encourage active travel in the context of developing health impact assessment (HIA) models to help decision-makers propose better solutions for healthy environments. We identify important components of HIA models of modal shifts in active travel in response to transport policies and interventions. RESULTS AND DISCUSSION Policies that increase active travel are likely to generate large individual health benefits through increases in physical activity for active travelers. Smaller, but population-wide benefits could accrue through reductions in air and noise pollution. Depending on conditions of policy implementations, risk tradeoffs are possible for some individuals who shift to active travel and consequently increase inhalation of air pollutants and exposure to traffic injuries. Well-designed policies may enhance health benefits through indirect outcomes such as improved social capital and diet, but these synergies are not sufficiently well understood to allow quantification at this time. CONCLUSION Evaluating impacts of active travel policies is highly complex; however, many associations can be quantified. Identifying health-maximizing policies and conditions requires integrated HIAs.

Commuters’ Exposure to Particulate Matter Air Pollution Is Affected by Mode of Transport, Fuel Type, and Route

Background Commuters are exposed to high concentrations of air pollutants, but little quantitative information is currently available on differences in exposure between different modes of transport, routes, and fuel types. Objectives The aim of our study was to assess differences in commuters’ exposure to traffic-related air pollution related to transport mode, route, and fuel type. Methods We measured particle number counts (PNCs) and concentrations of PM2.5 (particulate matter ≤ 2.5 μm in aerodynamic diameter), PM10, and soot between June 2007 and June 2008 on 47 weekdays, from 0800 to 1000 hours, in diesel and electric buses, gasoline- and diesel-fueled cars, and along two bicycle routes with different traffic intensities in Arnhem, the Netherlands. In addition, each-day measurements were taken at an urban background location. Results We found that median PNC exposures were highest in diesel buses (38,500 particles/cm3) and for cyclists along the high-traffic intensity route (46,600 particles/cm3) and lowest in electric buses (29,200 particles/cm3). Median PM10 exposure was highest from diesel buses (47 μg/m3) and lowest along the high- and low-traffic bicycle routes (39 and 37 μg/m3). The median soot exposure was highest in gasoline-fueled cars (9.0 × 10−5/m), diesel cars (7.9 × 10−5/m), and diesel buses (7.4 × 10−5/m) and lowest along the low-traffic bicycle route (4.9 × 10−5/m). Because the minute ventilation (volume of air per minute) of cyclists, which we estimated from measured heart rates, was twice the minute ventilation of car and bus passengers, we calculated that the inhaled air pollution doses were highest for cyclists. With the exception of PM10, we found that inhaled air pollution doses were lowest for electric bus passengers. Conclusions Commuters’ rush hour exposures were significantly influenced by mode of transport, route, and fuel type.

Respiratory health effects of ultrafine and fine particle exposure in cyclists

Objectives Monitoring studies have shown that commuters are exposed to high air pollution concentrations, but there is limited evidence of associated health effects. We carried out a study to investigate the acute respiratory health effects of air pollution related to commuting by bicycle. Methods Twelve healthy adults cycled a low- and a high-traffic intensity route during morning rush hour in Utrecht, The Netherlands. Exposure to traffic-related air pollution was characterised by measurements of PM10, soot and particle number. Before, directly after and 6 h after cycling we measured lung function (FEV1, FVC, PEF), exhaled NO (FENO) and respiratory symptoms. The association between post- minus pre-exposure difference in health effects and exposure during cycling was evaluated with linear regression models. Results The average particle number concentration was 59% higher, while the average soot concentration was 39% higher on the high-traffic route than on the low-traffic route. There was no difference for PM10. Contrary to our hypothesis, associations between air pollution during cycling and lung function changes immediately after cycling were mostly positive. Six hours after cycling, associations between air pollution exposure and health were mostly negative for lung function changes and positive for changes in exhaled NO, although non-significant. Conclusions We found substantial differences in ultrafine particle number and soot exposure between two urban cycling routes. Exposure to ultrafine particles and soot during cycling was weakly associated with increased exhaled NO, indicative of airway inflammation, and decrements in lung function 6 h after exposure. A limitation of the study was the relatively small sample size.

Cadmium and children: exposure and health effects.

Cadmium exposure and accumulation in the body start at young age. Exposure routes in children are mainly via food, environmental tobacco smoke and house dust. Excretion from the body is limited. Cadmium accumulation in the kidney is responsible for effects such as nephrotoxicity and osteoporosis which are observed at adult age. Cadmium exposure through inhalation is also associated with lung cancer in adulthood. Although transfer to the neonate through the placenta and through breast milk is limited, teratogenic and developmental effects were observed in experimental animals. The database on human studies involving children is limited, yet effects on motoric and perceptual behaviour in children have been associated with elevated in utero cadmium exposure. In school age children urinary cadmium levels were associated with immune suppressive effects. More studies are needed to confirm these results. Experimental data in vitro and in animals refer to effects of cadmium on the hypothalamus‐pituitary axis at different levels. This may lead to disorders of the endocrine and/or immune system. Cadmium exposure at early age should be limited as much as possible to prevent direct effects on children and to prevent accumulation of cadmium which may have serious health effects only becoming manifest at older age.

Respiratory Effects of Commutersʼ Exposure to Air Pollution in Traffic

Background: Much time is spent in traffic, especially during rush hours, when air pollution concentrations on roads are relatively high. Controlled exposure studies have shown acute respiratory effects of short, high exposures to air pollution from motor vehicles. Acute health effects of lower real-life exposures in traffic are unclear. Methods: Exposures of 34 healthy, nonsmoking adult volunteers were repeatedly measured while commuting for 2 hours by bus, car, or bicycle. Particle number (PN), particulate matter (PM2.5 and PM10), and soot exposures were measured. Lung function and airway resistance were measured directly before, directly following, and 6 hours after exposure. Exhaled nitric oxide (NO) was measured directly before and 6 hours after exposure. Inhaled doses were estimated based on monitored heart rates. Mixed models were used to analyze effects of exposure on changes in health parameters after exposure compared with before. Results: PN, PM10, and soot were associated with decreased peak expiratory flow directly following but not 6 hours after exposure. PN doses were associated with decreases in maximum midexpiratory flow and forced expiratory flow (FEV1) 6 hours after exposure, whereas PN and soot exposures were associated with increased maximum midexpiratory flow and FEV1 directly after exposure. PN and soot were associated with increased exhaled NO after car and bus but not bicycle trips. PN was also associated with an increase in airway resistance directly following exposure but not 6 hours later. Conclusions: We found modest effects of 2-hour in-traffic exposure to air pollutants on peak flow, exhaled NO, and airway resistance.

In-Traffic Air Pollution Exposure and CC16, Blood Coagulation, and Inflammation Markers in Healthy Adults

Background: Exposure to traffic-related air pollution is a risk factor for cardiovascular events, probably involving mechanisms of inflammation and coagulation. Little is known about effects of the short exposures encountered while participating in traffic. Objectives: The objective of the study was to examine effects of exposure of commuters to air pollution on cardiovascular biomarkers. Methods: Thirty-four healthy adult volunteers commuted for 2 hr by bus, car, or bicycle during the morning rush hour. During the commute, exposure to particle number, particulate matter (PM) ≤ 2.5 µm in aerodynamic diameter (PM2.5), PM ≤ 10 µm in diameter (PM10), and soot was measured. We estimated inhaled doses based on heart rate monitoring. Shortly before exposure and 6 hr after exposure, blood samples were taken and analyzed for CC16 (Clara cell protein 16), blood cell count, coagulation markers, and inflammation markers. Between June 2007 and June 2008, 352 pre- and postexposure blood samples were collected on 47 test days. We used mixed models to analyze the associations between exposure and changes in health parameters. Results: We observed no consistent associations between the air pollution exposures and doses and the various biomarkers that we investigated. Conclusions: Air pollution exposure during commuting was not consistently associated with acute changes in inflammation markers, blood cell counts, or blood coagulation markers.

The effects of PCBs and dioxins on child health

Background/exposure: Dioxins and PCBs are highly persistent and highly toxic environmental pollutants which at present are derived mainly from waste incineration and food contamination. They are widespread in nature and pollute human food, including breast milk so that basically all children in Europe are exposed to measurable levels. Results/toxicity in children: The toxicity of dioxins and PCBs are well described both from animal studies and from a number of human epidemiological studies including several large cohort studies. Especially developmental exposure has been shown to affect endocrine and cognitive systems negatively. Measurable outcomes include reduced IQ and changed behaviour. Foetotoxic effects with reduced birth weight and increased congenital anomalies such as cleft lip have also been described. Exposure to PCBs and dioxins must be considered also in the context of multiple exposure to several toxins simultaneously or sequentially.

Exposure to multiple environmental agents and their effect

Introduction: All children are exposed to multiple physical, chemical and biological challanges that can result in adverse health effects before and after birth. In this context, the danger of multiple exposures cannot be assessed from a single‐chemical approach as used in classical toxicology. Aim: To open up a ‘negotiation space’ for the problem of multiple exposure to environmental stressors, defined as any physical, chemical or biological entity that can induce an adverse response. In this context, two further questions obtain: to what extent can synergistic risks be assessed, and how far could potential adverse effects be prevented by enhanced regulation?Methods: A discussion of two general approaches is taken: 1 ) the investigation of mixtures such as smoking or air pollution without specifying the individual agents, and 2 ) the investigation of individual substances with a focus on possible interactions in the context of dose to receptor. Results: Although mixtures of compounds can have effects, it may not be possible to ascribe causation to a single compound. Furthermore, cumulative low‐dose insult can, in some circumstances, be more toxic than a single high‐dose exposure, e.g. endocrine disruptive effects of a combination of PCBs and dioxins which disrupt the thyroid hormone status; this tends to contradict elements of classical toxicology,. These cumulative insults may further combine with heavy metals and can disrupt the heme synthesis. It is possible that groups of pollutants could be used to test their cumulative capacity to multiple stress‐susceptible receptor targets as is done in smoking and air pollution. This methodology could be used for further groups of potential pollutants, for example those associated with cleaning products, or cosmetics. Testing individual substances with a focus on interactions means that not only chemicals but also concurrent diseases should be taken into account. We suggest that the enhanced regulation of potential multiple stressors falls into two discrete categories. The first comprises a more precautionary approach (as demonstrated by the banning of chemicals such as some brominated flame retardants in Europe). The second comprises a more ‘permissive’ liberal approach involving the initial study of an individual compound, and subsequent interrogation of that compound in combination with another (as demonstrated by lowering the carcinogenicity of aflatoxin by vaccination against hepatitis B).

Children's exposure to polybrominated diphenyl ethers

Background: Polybrominated biphenyl ethers (PBDEs), a class of brominated flame retardants, are frequently used in consumer products. PBDEs levels in environmental and human samples have increased in recent decades. Children are exposed to PBDEs through diet, mainly through fish, meat and milk. Total dietary exposure of children in Europe was calculated to be 2–3 ng/kg b.w./day. For nursing infants the main source of PBDE exposure is breast milk; exposure levels are around 15 ng/kg b.w./day. PBDE exposure levels in North America are 10 to a 100 times higher. Because of their persistence and their similarity to polychlorinated biphenyls (PCBs), concern has been raised about the effects of PBDEs on human health. Exposure to penta‐ and octa‐BDE led to learning impairment and impaired motor behaviour in rodents. Exposure to penta‐, octa‐ and also deca‐BDE caused effects on thyroid homeostasis in animals.

Today's epidemics in children: possible relations to environmental pollution and suggested preventive measures.

Background: Facts and hypotheses on the relationship between some childrens diseases or disorders and external stressors during the developmental stage of a child, both prenatally and postnatally are described in literature. In this paper the following changes in patterns and causes of the main childhood illnesses are summarized and recommendations for actions are made.