Part,  Chapter, Paragraph

  1    -,     1        |           factors through a number of exposure routes and many different
  2    I,     2.  1    |           animals has broadened human exposure to a variety of micro-organisms
  3    I,     2.  2    |             broadens human and animal exposure to a variety of biological
  4    I,     2.  2    |           other goods broadened human exposure to a variety of hazardous
  5    I,     2.  5    |       Rantanen, 1998). The use of and exposure to new technological products,
  6    I,     2.  7    |   occupational backgrounds, and their exposure to environmental conditions.
  7    I,     2.  8    |               long terni effects from exposure during mining.~ ~Minimal (
  8    I,     2.  8    | responsibility of the enterprise. The exposure of the local population
  9    I,     2. 10.  1|               health data such as the exposure to toxic substances (toxicogenomics)
 10   II,     5.  1.  1|          intake, lack of exercise and exposure to stress, remains essential
 11   II,     5.  1.  1|              age, after many years of exposure to unhealthy lifestyle (
 12   II,     5.  1.  1|                although pollution and exposure to certain gases/chemicals
 13   II,     5.  1.  1|      mortality are influenced by past exposure to tobacco smoking, and
 14   II,     5.  1.  1|              nervous system disorders~Exposure in utero or during development
 15   II,     5.  1.  1|    development of cognitive function. Exposure to polychlorinated biphenyls (
 16   II,     5.  1.  1|           policies at the moment are: exposure to allergens (pollen, fungal
 17   II,     5.  1.  1|             and tobacco environmental exposure; indoor and outdoor air
 18   II,     5.  1.  1|            gluten associated with the exposure to foods containing wheat,
 19   II,     5.  1.  1|             dermatitis (e.g. frequent exposure to mild irritant soaps seen
 20   II,     5.  1.  1|          development can be caused by exposure to lead, cadmium, mercury,
 21   II,     5.  2.  2|              age, after many years of exposure to unhealthy lifestyle (
 22   II,     5.  3.  2|             mesothelioma is caused by exposure to asbestos;~- lymphoma
 23   II,     5.  3.  4|                although pollution and exposure to certain gases/chemicals
 24   II,     5.  3.  4|      mortality are influenced by past exposure to tobacco smoking, and
 25   II,     5.  3.  5|            have similar HPV infection exposure and the organised screening
 26   II,     5.  3.  5|               caused by different HPV exposure and by the different introduction
 27   II,     5.  3.  7|              of the disease. Avoiding exposure to risk determinants would
 28   II,     5.  5.  2|             measures include reducing exposure to factors which might cause
 29   II,     5.  5.  2|       nevertheless be taken to reduce exposure to risk factors which can
 30   II,     5.  5.  3|               eating disorders is the exposure to Western media and its
 31   II,     5.  5.  3|         distribution of environmental exposure specify to what was hypothesized.~
 32   II,     5.  5.  3|              status with diet and sun exposure, early life infections including
 33   II,     5.  5.  3|               proposed, but no single exposure has been consistently implicated (
 34   II,     5.  5.  3|            agreement that smoking and exposure to pesticide affect the
 35   II,     5.  8.  1|              or gases (GOLD, 2006).~ ~Exposure to noxious agents (e.g.
 36   II,     5.  8.  4|           concluded that occupational exposure contributes by about 10-
 37   II,     5.  9. FB|               in response to ordinary exposure to low doses of allergens,
 38   II,     5.  9. FB|             of IgE in response to the exposure to substances that usually
 39   II,     5.  9. FB|        awareness of these conditions, exposure to indoor and outdoor pollutants
 40   II,     5.  9. FB|               particular, the reduced exposure to microbes seen in Europe
 41   II,     5.  9. FB|            and have a low cost.~ ~All exposure to tobacco smoke should
 42   II,     5.  9. FB|              or cockroaches, specific exposure should be reduced or abolished
 43   II,     5.  9. FB|           employees from occupational exposure if they have developed symptoms
 44   II,     5.  9.  1|           nose induced after allergen exposure. Symptoms of allergic rhinitis
 45   II,     5.  9.  1|       attributed mainly to changes in exposure to environmental risk factors
 46   II,     5.  9.  4|               at the moment are:~ ~1. exposure to allergens and sensitization;~
 47   II,     5.  9.  4|             and tobacco environmental exposure;~3. indoor and outdoor pollution;~
 48   II,     5.  9.  4|        symptoms are determined by the exposure to chemical or biologic
 49   II,     5.  9.  4|              investigated the role of exposure to substances in the workplace
 50   II,     5.  9.  4|            asthma risk was seen after exposure to substances known to cause
 51   II,     5.  9.  4|          their references.~ ~Allergen exposure has been linked to the development
 52   II,     5.  9.  4|         relationship between allergen exposure and allergic sensitization
 53   II,     5.  9.  4|           allergen doses, duration of exposure and maybe also an individual,
 54   II,     5.  9.  4|       prevalence of sensitization and exposure to high levels of the epitope
 55   II,     5.  9.  4|         Simpson , 2005; Erwin, 2005). Exposure to house dust mite or cat
 56   II,     5.  9.  4|               be due to variations in exposure in some large countries (
 57   II,     5.  9.  4|            smoking in the EU. Tobacco exposure, in fact, is associated
 58   II,     5.  9.  4|          workers experiencing chronic exposure to gases, fumes, and biological
 59   II,     5.  9.  4|             and other children; early exposure to certain bacteria actually
 60   II,     5.  9.  4|             with air-pollution-linked exposure to PAHs.~ ~Another project (
 61   II,     5.  9.  5|              moment are:~· allergenic exposure and sensitization;~· cigarette
 62   II,     5.  9.  5|             and tobacco environmental exposure;~· indoor and outdoor pollution;
 63   II,     5.  9.  7|           mite, cat, and dog allergen exposure, pet ownership, and sensitization
 64   II,     5.  9.  7|                  2008): Tobacco smoke exposure and tracking of lung function
 65   II,     5.  9.  7|           McCusker C (2006): Neonatal exposure with LPS and/or allergen
 66   II,     5. 10.  1|        between environmental factors (exposure) and personal susceptibility (
 67   II,     5. 10.  1|               FA lies in the level of exposure to cross-reactive allergens (
 68   II,     5. 10.  3|           differences in potential of exposure, cross-reactivity with environmental
 69   II,     5. 10.  3|            gluten associated with the exposure to foods containing wheat,
 70   II,     5. 10.  5|               intolerance is avoiding exposure to the incriminated food,
 71   II,     5. 11.  3|           structure and its permanent exposure to environmental influences.
 72   II,     5. 11.  3|               related to occupational exposure, whereas the term eczema
 73   II,     5. 11.  3|             dermatitis (e.g. frequent exposure to mild irritant soaps seen
 74   II,     5. 11.  3|       piercing, where the duration of exposure may occur for an entire
 75   II,     5. 11.  3|              entire life, the chronic exposure to a low concentration of
 76   II,     5. 11.  3|              increased cumulative sun exposure and increasing incidence
 77   II,     5. 11.  3|               cumulative lifetime sun exposure (Rosso et al, 1996). NMSC
 78   II,     5. 11.  3|               to an increased leisure exposure to the sun. It is estimated
 79   II,     5. 11.  5|      behaviour to avoid excessive sun exposure, to recognise the visible
 80   II,     5. 12.  7|             al (1989): Decline in the exposure to hepatitis A and B infections
 81   II,     6.  3.  4|      infection with SARS-CoV would be exposure in laboratories where the
 82   II,     6.  3.  6|               infected through direct exposure to faeces from infected
 83   II,     6.  3.  7|             follow direct or indirect exposure to an infected animal’s
 84   II,     6.  3.  7|          vaccination (before or after exposure). Preventive veterinary
 85   II,     6.  4.  5|               into consideration that exposure to antimicrobial agents
 86   II,     7.  1    |           lesion resulting from acute exposure to energy (mechanical, thermal,
 87   II,     7.  1    |           freezing). The time between exposure and the appearance of the
 88   II,     7.  3.  4|         relationship between risk and exposure has recently been explored
 89   II,     7.  4    |              are also inequalities in exposure to injury risks according
 90   II,     8.  2.  1|     infections such as meningitis, or exposure to lead, mercury, and other
 91   II,     8.  2.  3|           loss due to ageing or noise exposure, which excludes hearing
 92   II,     8.  2.  3|        occupations with greater noise exposure. In Denmark and Finland,
 93   II,     9        |            during pregnancy. Prenatal exposure to alcohol can be associated
 94   II,     9        |             mutation, and under 5% to exposure to a single environmental
 95   II,     9        |             knowledge of the risks of exposure to chemicals, in the occupational,
 96   II,     9        |    precautionary approach in reducing exposure particularly to byproducts
 97   II,     9        |                although pollution and exposure to certain gases/chemicals
 98   II,     9.  1.  2|              that it can be caused by exposure to endocrine disrupting
 99   II,     9.  1.  2|            during pregnancy. Prenatal exposure to alcohol can be associated
100   II,     9.  1.  2|             mutation, and under 5% to exposure to a single environmental
101   II,     9.  1.  2|             knowledge of the risks of exposure to chemicals, in the occupational,
102   II,     9.  1.  2|    precautionary approach in reducing exposure particularly to byproducts
103   II,     9.  1.  2|              infection, maternal drug exposure, occupational exposures
104   II,     9.  1.  2|               L, for the Occupational Exposure and Congenital Malformations
105   II,     9.  1.  2|             and Maternal Occupational Exposure to Glycol Ethers", Epidemiology,
106   II,     9.  1.  2|                 Maternal Occupational Exposure and Congenital Malformations",
107   II,     9.  3.  1|                although pollution and exposure to certain gases/chemicals
108  III,    10.  1    |                 Important elements of exposure and risk assessment are
109  III,    10.  1    |               Late responses to early exposure' needs to be addressed,
110  III,    10.  1    |           individual and generational exposure and their effect. Preventive
111  III,    10.  1    |          Health determinants: agents, exposure routes, human settlements
112  III,    10.  1    |           influencing health~ ~AGENTS~EXPOSURE ROUTES~LIVING AND WORKING
113  III,    10.  1.  1|              usehealth determinant.~Exposure to second hand smoke and
114  III,    10.  1.  1|                 In addition, only the exposure to high-fat, low-carbohydrate
115  III,    10.  1.  3|            Active and passive tobacco exposure: a serious pediatric health
116  III,    10.  2.  1|               the environmental smoke exposure were published in the “Lifting
117  III,    10.  2.  1|            biomarkers for involuntary exposure to tobacco, such as serum
118  III,    10.  2.  1|              reflects the decrease in exposure on ETS due to anti-smoking
119  III,    10.  2.  1|              brain. Immediately after exposure to nicotine, there is a “
120  III,    10.  2.  1|       taxation);~· measures to reduce exposure to environmental tobacco smoke (
121  III,    10.  2.  1|               tobacco consumption and exposure to tobacco smoke.' The EU
122  III,    10.  2.  1|           measures;~· protection from exposure to tobacco smoke, particularly
123  III,    10.  2.  1|           Consequences of Involuntary Exposure to Tobacco Smoke A Report
124  III,    10.  2.  1|              TF (2006): Trends in the Exposure of Non smokers in the US
125  III,    10.  2.  1|              grey matter.~ ~Long term exposure to alcohol increases the
126  III,    10.  2.  1|               a carcinogen; long term exposure increases the risk of cancers
127  III,    10.  2.  1|       reproductive toxicity. Prenatal exposure to alcohol can be associated
128  III,    10.  2.  1|              advertisements and media exposure increase the likelihood
129  III,    10.  2.  1|          countries with inappropriate exposure to fluorides imply higher
130  III,    10.  2.  1|             but was not influenced by exposure to water fluoridation.~ ~
131  III,    10.  2.  1|        screening tool for preliminary exposure assessments by the EFSA
132  III,    10.  2.  1|            subject’s personal habits, exposure to sunlight can be too low
133  III,    10.  2.  4|               health data such as the exposure to toxic substances (toxico-genomics)
134  III,    10.  2.  4|           variants and the individual exposure to exogenous risks. In the
135  III,    10.  2.  5|          studies indicate the role of exposure during early life stages
136  III,    10.  2.  5|         vulnerability).~ ~For example exposure to chemicals during early
137  III,    10.  2.  5|           adult life after peri-natal exposure. It is concluded that exposure
138  III,    10.  2.  5|        exposure. It is concluded that exposure to chemicals with a mutagenic
139  III,    10.  2.  5|              not involved. Early life exposure to substances with estrogenic
140  III,    10.  2.  5|           ability of the organism, by exposure to toxic and carcinogenic
141  III,    10.  2.  5|            2003): Effect of antenatal exposure to maternal smoking on behaviournal
142  III,    10.  2.  5|               2007): Prenatal smoking exposure and psychiatric symptoms
143  III,    10.  3.  1|           sound pressure level.~LaeqT~Exposure to noise for the duration
144  III,    10.  3.  1|               noise. Radiation, radon exposure and noise have well documented
145  III,    10.  3.  1|               consider differences in exposure for different vulnerable
146  III,    10.  3.  1|         fields (EMF) but whether such exposure is causing any adverse effects
147  III,    10.  3.  1|            the radioactive gas radon. Exposure to radon increases significantly
148  III,    10.  3.  1|             connected to an increased exposure to UV-radiation. The currently
149  III,    10.  3.  1|              than 10 years and longer exposure times could be needed before
150  III,    10.  3.  1|             future magnitude of noise exposure is the growth in traffic
151  III,    10.  3.  1|           European Commission, 2002), exposure to noise has recently started
152  III,    10.  3.  1|              harmful effects of noise exposure. Not only does it require
153  III,    10.  3.  1|             on 21 March 2007.~ ~Noise exposure data has until now been
154  III,    10.  3.  1|           have gathered data on noise exposure as well as on noise annoyance.~ ~
155  III,    10.  3.  1|      annoyance.~ ~At the moment noise exposure data is produced and reported
156  III,    10.  3.  1|         inform the public about noise exposure and its effects, and to
157  III,    10.  3.  1|           important pathway for human exposure is permeation of radon gas
158  III,    10.  3.  1|               contribute to the total exposure. Radon decays to radon daughters,
159  III,    10.  3.  1|           strong relationship between exposure to radon and the development
160  III,    10.  3.  1|              that in the Netherlands, exposure to radon in dwellings leads
161  III,    10.  3.  1|              can be ascribed to radon exposure per year (Barns, 2005).
162  III,    10.  3.  1|   epidemiological studies on domestic exposure to radon establishes a clear
163  III,    10.  3.  1|           risk and the level of radon exposure (Darby et al, 2005). The
164  III,    10.  3.  1|              effect of radon daughter exposure and smoking is multiplicative (
165  III,    10.  3.  1|              risk associated to radon exposure. With the numbers presented
166  III,    10.  3.  1|             is not known if childhood exposure to radon increases the risk
167  III,    10.  3.  1|          confirm this.~ ~Indoor radon exposure caused by radon gas seeping
168  III,    10.  3.  1|               Another source of radon exposure is building materials. Exposure
169  III,    10.  3.  1|       exposure is building materials. Exposure is reduced by routine radon
170  III,    10.  3.  1|          likely increase indoor radon exposure. Almost all European countries
171  III,    10.  3.  1|        remediation to reduce children exposure. Very few countries explicitly
172  III,    10.  3.  1|              between skin cancers and exposure to UV radiation (UVR). UVR
173  III,    10.  3.  1|               factors influencing UVR exposure intensity such as latitude,
174  III,    10.  3.  1|               is that sunlight and UV exposure stimulates the synthesis
175  III,    10.  3.  1|             to increased ground level exposure to UVR in recent years.
176  III,    10.  3.  1|            possible health effects of exposure to low intensity Radio Frequency
177  III,    10.  3.  1|          consistently demonstrated at exposure levels below the limits
178  III,    10.  3.  1|               for long-term low-level exposure.~ ~For Intermediate Frequency
179  III,    10.  3.  1|         health effects from long-term exposure to IF fields are important
180  III,    10.  3.  1|               important because human exposure to these fields is increasing
181  III,    10.  3.  1|         controls) suggested that “the exposure to EMF in the workplace
182  III,    10.  3.  1|              relation to occupational exposure.~ ~The balance of epidemiologic
183  III,    10.  3.  1|            more sensitive to RF field exposure than adults in view of their
184  III,    10.  3.  1|              a much higher cumulative exposure than previous generations.
185  III,    10.  3.  1|               currently available. RF exposure has not consistently been
186  III,    10.  3.  1|         indicated any health risks at exposure levels below the ICNIRP-limits
187  III,    10.  3.  1|              scarcity of data at high exposure levels. There is no consistent
188  III,    10.  3.  1|           affect cells at non-thermal exposure level. In conclusion, no
189  III,    10.  3.  1|          consistently demonstrated at exposure levels below the ICNIRP-limits
190  III,    10.  3.  1|               for long-term low-level exposure.~ ~Combined analyses of
191  III,    10.  3.  1|               the association between exposure to ELF and childhood leukaemia
192  III,    10.  3.  1|               some inconsistencies in exposure measurements and the absence
193  III,    10.  3.  1|        Whether changes of recommended exposure limits to 50/60 Hz magnetic
194  III,    10.  3.  1|               clues for reconsidering exposure limits. Reports on possibly
195  III,    10.  3.  1|              proposing changes in the exposure limits.”~ ~Noise~ ~Since
196  III,    10.  3.  1|           limited evidence available, exposure to leisure time noise in
197  III,    10.  3.  1|           normal cognitive processes. Exposure of the pregnant mother to
198  III,    10.  3.  1|               of disease due to noise exposure (Knol et al., 2005; Torfs,
199  III,    10.  3.  1|   cardiovascular disease due to noise exposure is considerable as shown
200  III,    10.  3.  1|    attributable to road traffic noise exposure (Babisch, 2006).~ ~Figure
201  III,    10.  3.  1|        population live in areas where exposure limits of traffic noise
202  III,    10.  3.  1|              in 1986) to reduce noise exposure from traffic infrastructure,
203  III,    10.  3.  1|           existing estimates of noise exposure in Europe cover either the
204  III,    10.  3.  1|             necessary to assess noise exposure. Improvements are expected
205  III,    10.  3.  1|               exposed to noise. Noise exposure information will geographically
206  III,    10.  3.  1|             of combined environmental exposure should be facilitated.~ ~
207  III,    10.  3.  1|               10.3.1.1. Self-reported exposure to physical risk factors
208  III,    10.  3.  1|           public against indoor radon exposure (90/143/Euratom). This Recommendation
209  III,    10.  3.  1|               a person’s lifetime UVR exposure occurs before the age of
210  III,    10.  3.  1|               protected from high UVR exposure, whilst babies should always
211  III,    10.  3.  1|     consulting the public about noise exposure, its effects, and the measures
212  III,    10.  3.  1|               significant increase in exposure due to natural radiation
213  III,    10.  3.  1|           reduce children's excessive exposure to UVR. Excessive solar
214  III,    10.  3.  1|              UVR. Excessive solar UVR exposure is best prevented by regional
215  III,    10.  3.  1|              major sources. The noise exposure information from Member
216  III,    10.  3.  1|              Risk assessment of noise exposure - the Swiss perspective.
217  III,    10.  3.  1|             association between noise exposure and blood pressure and ischemic
218  III,    10.  3.  1|             cancer risk associated to exposure to radon and smoking in
219  III,    10.  3.  1|               Pa (2007): Occupational exposure to Electromagnetic Field
220  III,    10.  3.  1|             2007). Guidelines for the exposure to noise at night. Edited
221  III,    10.  3.  2|            releases causing long-term exposure to low levels of chemical
222  III,    10.  3.  2|         children. The threats include exposure to natural or human-made
223  III,    10.  3.  2|             global climate change and exposure to chemicals that disrupt
224  III,    10.  3.  2|          chemical flow and widespread exposure with potentially adverse
225  III,    10.  3.  2|              and thereby increase the exposure to them of both people and
226  III,    10.  3.  2|      nanotechnology; newly identified exposure routes such as the case
227  III,    10.  3.  2|          spraying leading to chemical exposure of people living nearby
228  III,    10.  3.  2|               Due to the lack of good exposure data and patchy information
229  III,    10.  3.  2|          studies indicate the role of exposure during early life stages
230  III,    10.  3.  2|         concerning neurodevelopment; “Exposure to chemicals during early
231  III,    10.  3.  2|            adult life after perinatal exposure (Barton et al, 2005; EHP,
232  III,    10.  3.  2|           2006). It is concluded that exposure to chemicals with a mutagenic
233  III,    10.  3.  2|              not involved. Early life exposure to substances with estrogenic
234  III,    10.  3.  2|          bodyweight per day. The main exposure route for humans is food (
235  III,    10.  3.  2|      legislation for preventing human exposure. However, they may reach
236  III,    10.  3.  2|              increasing environmental exposure and of their suspected carcinogenicity.~ ~
237  III,    10.  3.  2|          inter alia, prenatal mercury exposure and to ensure that tolerable
238  III,    10.  3.  2|          humans suggest that a ‘safeexposure level currently cannot be
239  III,    10.  3.  2|        established. More data on lead exposure of European citizens are
240  III,    10.  3.  2|           clearly indicates a reduced exposure.~ ~Biomonitoring~ ~Every
241  III,    10.  3.  2|               good indicator of human exposure to persistent chemicals
242  III,    10.  3.  2|               used as an indicator of exposure. The bio-monitoring of different
243  III,    10.  3.  2|                as well as on combined exposure from different media, sources
244  III,    10.  3.  2|        susceptibility from early-life exposure to carcinogens. Environm.
245  III,    10.  3.  2|              children associated with exposure to chemicals. Geneva, World
246  III,    10.  3.  4|         mortality from decreased cold exposure~Increase in frequency of
247  III,    10.  3.  4|        thereby heat elimination. Heat exposure can increase medication
248  III,    10.  3.  4|        buildings, indoor temperature, exposure to a high concentration
249  III,    10.  3.  4|              periods. Accidental cold exposure occurs mainly outdoors,
250  III,    10.  3.  4|           acute or chronic effects of exposure to chemical pollutants released
251  III,    10.  3.  4|          European Region, 19902006~ ~Exposure to flooding reportedly results
252  III,    10.  4    |                                 10.4. EXPOSURE ROUTES~ ~
253  III,    10.  4.  1|           values.~ ~Long-term average exposure to particulate matters (
254  III,    10.  4.  1|             in adults. The measure of exposure combines the PM10 concentration
255  III,    10.  4.  1|             population subject to the exposure.~Most (89%) people (including
256  III,    10.  4.  1|              1.2 shows the changes in exposure occurred in cities in the
257  III,    10.  4.  1|               the distribution of the exposure of children based on the
258  III,    10.  4.  1|              both short and long-term exposure. Many studies show that
259  III,    10.  4.  1|          months for every EU citizen. Exposure to PM is also linked to
260  III,    10.  4.  1|             and asthmatic problems of exposure to emissions from moisture
261  III,    10.  4.  1|             CBA included:~ ~· Chronic exposure:~o Mortality (PM) – the
262  III,    10.  4.  1|             bronchitis (PM)~ ~· Acute exposure (daily variations)~o Mortality (
263  III,    10.  4.  1|               levels, since long-term exposure accounts for the majority
264  III,    10.  4.  2|             Term Intake~MOE~Margin of Exposure~MRLs~Maximum Residue Limits~
265  III,    10.  4.  2|         networks for events involving exposure to radio-chemicals or unsafe
266  III,    10.  4.  2|               levels required for the exposure assessment. There is thus
267  III,    10.  4.  2|             be representative for the exposure of the general population.~ ~
268  III,    10.  4.  2|              actual dietary pesticide exposure throughout Europe. The programme
269  III,    10.  4.  2|           Occurrence~Trend~Main human exposure route~ ~ ~ ~ ~Campylobacteriosis~
270  III,    10.  4.  2|              Existing legal standard ~Exposure, possible~exceedance of
271  III,    10.  4.  2|              Possibility to influence~exposure~Remarks, sources~ ~Substances
272  III,    10.  4.  2|           meat~ ~At current levels of~exposure, natural growth~promoters
273  III,    10.  4.  2|               detected; sporadic high~exposure when injection~site is consumed~
274  III,    10.  4.  2|              preparation~Current oral exposure in~ the Netherlands to PAHs, ~
275  III,    10.  4.  2|             Genotoxic carcinogen~None~Exposure or actual effects~unknown~
276  III,    10.  4.  2|       standards~for various foods~ ~ ~Exposure reduced by~measures; estimate
277  III,    10.  4.  2|                 Little is known about~exposure in the Dutch~situation;
278  III,    10.  4.  2|               environmental and human exposure in areas far from where
279  III,    10.  4.  2|        considerable decrease of human exposure to dioxin-like compounds
280  III,    10.  4.  2|              led in September 1997 to exposure of workers and leakage into
281  III,    10.  4.  2|             is a major route of human exposure; however, there is currently
282  III,    10.  4.  2|              on pesticide residues.~ ~Exposure to a mixture of compounds
283  III,    10.  4.  2|          weaker than expected effect. Exposure to multiple residues of
284  III,    10.  4.  2|         body weight per day. The main exposure route for humans is food (
285  III,    10.  4.  2|           health arising from nitrate exposure. No new hazard data were
286  III,    10.  4.  2|              kg b.w) (FAO/WHO, 2003). Exposure estimates were made by combining
287  III,    10.  4.  2|             leafy vegetables, nitrate exposure was just above or below
288  III,    10.  4.  2|              Existing legal standard ~Exposure, possible~exceedance of
289  III,    10.  4.  2|              Possibility to influence~exposure~Remarks, sources~‘Normal290  III,    10.  4.  2|            baby food~in preparation~ ~Exposure below the~standard; the
291  III,    10.  4.  2|               wine in preparation~ ~ ~Exposure well below the~human health-based
292  III,    10.  4.  2|             apple~juice/apple sauce~ ~Exposure below the~standard~ ~Monitoring~ ~
293  III,    10.  4.  2|     Oestrogenic effect~In preparation~Exposure below the standard~Monitoring~
294  III,    10.  4.  2|               cancer~ ~In preparation~Exposure below the standard~Monitoring~
295  III,    10.  4.  2|       Varieties List.~ ~Sporadic high exposure~Certain parts of the~potato
296  III,    10.  4.  2|             preparation~Sporadic high exposure~Monitoring~Speijers & van
297  III,    10.  4.  2|             spinach,~drinking water~ ~Exposure via drinking water,~below
298  III,    10.  4.  2|             derivation of a Margin of Exposure (MOE), i.e. the point selected
299  III,    10.  4.  2|           range to background dietary exposure relate to the uncertainties
300  III,    10.  4.  2|              measure of acute dietary exposure that is used in MRL-setting
301  III,    10.  4.  2|            basis for estimating acute exposure to pesticide residues.~While,
302  III,    10.  4.  2|           Toxicology:GD on Pesticides Exposure Assessment for Workers,
303  III,    10.  4.  2|              to carry out appropriate exposure assessments and evaluate
304  III,    10.  4.  2|              of pesticides in air and exposure assessment.~ ~European consultations
305  III,    10.  4.  2|        regarding compound and type of exposure (acute, chronic), guidelines
306  III,    10.  4.  2|              modelling and cumulative exposure assessment. Cooperation
307  III,    10.  4.  2|                 the third step is the exposure assessment. Here, the intake
308  III,    10.  4.  2|              characterization and the exposure assessment and evaluates
309  III,    10.  4.  2|            dose-response assessment), exposure assessment, and (probability
310  III,    10.  4.  2|               short-term or long-term exposure, and whether only certain
311  III,    10.  4.  2|         hazard to which a significant exposure may occur, from an unexpected
312  III,    10.  4.  2|              or increased significant exposure and/or susceptibility to
313  III,    10.  4.  2|           samples: Assessment of PFOS exposure in a susceptible population
314  III,    10.  4.  3|            cause of cancer. Long term exposure has furthermore been documented
315  III,    10.  4.  3|              is a potential for human exposure, especially in areas with
316  III,    10.  4.  4|             well as to the increasing exposure towards them for both people
317  III,    10.  4.  5|                      10.4.5. Multiple exposure: bathing water and soil
318  III,    10.  4.  5|            opportunities for multiple exposure of human beings when bathing,
319  III,    10.  4.  5|               to be associated to the exposure to toxic algae but primarily
320  III,    10.  4.  5|            Another potential risk for exposure is via the lungs when sea
321  III,    10.  4.  5|            from studies that consider exposure pathways and biomarkers
322  III,    10.  4.  5|               and biomarkers of human exposure and effect, and compare
323  III,    10.  4.  5|               specific conditions and exposure of the receptors. In fact,
324  III,    10.  4.  5|             zone etc.) as well as the exposure of the receptors (e.g. humans
325  III,    10.  4.  5|         groundwater resources and the exposure of humans via drinking water
326  III,    10.  4.  5|              land-filling lack direct exposure measurements of emitted
327  III,    10.  4.  5|            site or, in some cases, on exposure modelling; a number of health
328  III,    10.  4.  5|        lymphomas, possibly related to exposure to 2,3,7,8-TCDD and related
329  III,    10.  4.  5|  approximately 0.5%. In 2003, the WHO exposure assessment expert group
330  III,    10.  4.  5|      facilities and the mitigation of exposure to emissions and leachates
331  III,    10.  4.  5|       inequity in the distribution of exposure among population subgroups.~ ~
332  III,    10.  4.  5|            from studies that consider exposure pathways and biomarkers
333  III,    10.  4.  5|            pathways and biomarkers of exposure and effect, and compare
334  III,    10.  4.  5|            order to evaluate chemical exposure pathways and assess the
335  III,    10.  4.  5|               pathways and assess the exposure for specific subsets of
336  III,    10.  4.  5|             improved understanding of exposure pathways, before considering
337  III,    10.  5.  1|            the detailed mechanisms of exposure may be different. For example,
338  III,    10.  5.  1|            quality problems and noise exposure in many rural places but
339  III,    10.  5.  1|             2007). Within Europe, the exposure to damp and mould in the
340  III,    10.  5.  1|               prolong or increase the exposure to indoor pollutants and
341  III,    10.  5.  1|            higher and also that their exposure to certain CDs is higher.~ ~
342  III,    10.  5.  1|            avoid unnecessary chemical exposure.~ ~Building dampness and
343  III,    10.  5.  1|               to reduce noise and air exposure and also have a compensating
344  III,    10.  5.  1|               10% or more suffer from exposure to noise levels of 65 dBA.
345  III,    10.  5.  1|               with unacceptable noise exposure conditions, while for another
346  III,    10.  5.  1|               project show that noise exposure is a key problem especially (
347  III,    10.  5.  1|              bigger cities, where the exposure to increased noise levels
348  III,    10.  5.  1|               settlements suffer from exposure to industrial activities
349  III,    10.  5.  1|           Neighborhood Conditions and Exposure to Cockroaches in Three
350  III,    10.  5.  1|            relation to microbial dust exposure in schools in Taiyuan, China
351  III,    10.  5.  2|              of populations, or their exposure to environmental conditions.~ ~
352  III,    10.  5.  2|       pollution, water quality, noise exposure and access to green and
353  III,    10.  5.  3|              the EU15. With regard to exposure to bullying and/or harassment,
354  III,    10.  5.  3|             effects from such kind of exposure to a great extent .~All
355  III,    10.  5.  3|        working methods that need less exposure to noise~- the choice of
356  III,    10.  5.  3|         duration and intensity of the exposure through work scheduling~ ~
357  III,    10.  5.  3|            requirements regarding the exposure of workers to the risks
358  III,    10.  5.  3|            the risks related to noise exposure at work, setting a new daily
359  III,    10.  5.  3|             work, setting a new daily exposure limit value of 87 dB(A).~
360  III,    10.  6.  2|           social gradient.~The higher exposure of vulnerability towards
361   IV,    11.  6.  4|            modifies the effect of the exposure on the outcome of interest.
362   IV,    11.  6.  4|              relationship between the exposure and the outcome will be
363   IV,    12.  2    |       taxation);~· measures to reduce exposure to environmental tobacco smoke (
364   IV,    12.  2    |               tobacco consumption and exposure to tobacco smoke.' The EU
365   IV,    12.  2    |             measures;~protection from exposure to tobacco smoke, particularly
366   IV,    12.  2    |              advertisements and media exposure increase the likelihood
367   IV,    12.  5    |            information on hazards and exposure; foster integrated and harmonised
368   IV,    12. 10    |            and to prevent involuntary exposure to environmental tobacco smoke.~ ~
369   IV,    12. 10    |                  Limit values for the exposure to environmental noise are
370   IV,    12. 10    |             2008: reduce occupational exposure to CMRs~Special work-related
371   IV,    12. 10    |           tobacco use~ ~Self-reported exposure to second-hand tobacco smoke~
372   IV,    13.  2.  2|      retardation, resulting from lead exposure, accounted for 4% of DALYs.
373   IV,    13.  2.  3|               typically the result of exposure to hazards that are produced
374   IV,    13.  2.  3|       retardation resulting from lead exposure accounted for 4 % of DALYs.~ ~
375   IV,    13.  7.  3|         include health effects of the exposure to environmental stressors
376  Key,   Ap5.  0.  0|              expenditure~expenditures~exposure~exposures~extreme~eye~eyecare~