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Re: stoppani,il cromo arriva in spiaggia



Andrea ha scritto:


> Cromo e nichel sulla spiaggia di Cogoleto in quantità fino a cento 
volte
> superiori ai limiti consentiti dalla legge. Cromo, ferro, manganese, 
nichel
> e zinco, presenti massicciamente sui due versanti collinari della Val
> Lerone, fino a cento metri sul livello dei mare. La contaminazione da
> metalli pesanti, al confine tra le due cittadine rivierasche di 
Cogoleto ....etc..


La presenza di cosi' tanto Cromo e' *estremamente grave*
E' necessaria una notevole bonifica. La popolazione e' esposta a rischio 
di vari tipi di cancro (esistono dati epidemiologici?)

Il cromo e' un noto pericoloso agente cancerogeno.
Se ce ne fosse bisogno, includo (sotto) gli abstracts di un pugno dei 
molti articoli scientifici che trattano gli effetti cancerogeni e 
tossici del Cromo sia per i lavoratori che per la popolazione...

Spero interessi
Alessandro Gimona

ps qualcuno ha visto Erin Brockovich?


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Gibb HJ; Lees PSJ; Pinsky PF; Rooney BC  
  
Lung cancer among workers in chromium chemical production 
  
AMERICAN JOURNAL OF INDUSTRIAL MEDICINE 2000,   38,    2, pp 115-126 
  
Background An elevated risk of lung cancer among workers in chromate 
production facilities has previously beer? reported. This
excess risk is believed to be the result of exposure to hexavalent 
chromium, There have been mixed reports about whether trivalent
chromium exposure is also associated with an excess lung cancer risk. 
Previous studies of measured hexavalent chromium exposure
and lung cancer risk have not examined cigarette smoking as a risk 
factor: Methods ii cohort of 2,357 workers first employed between
1950 and 1974 at a chromate production plant was identified. Vital 
status of the workers was followed until December 31, 1992.
Work histories of cohort members were compiled from the beginning of 
employment through 1985, the year the plant closed. Annual
average exposure estimates, based on historical exposure measurements, 
were made for each job title in the plant for the years
1950-1985. These exposure estimates were used to calculate the 
cumulative hexavalent chromium exposure of each member of the
study population. Following closure of the plant, settled dust samples 
were collected and analyzed for hexavalent and trivalent
chromium. The trivalent/hexavalent concentration ratios in each plant 
area were combined with historic air-sampling data to estimate
cumulative trivalent chromium exposure for each individual in the study? 
cohort. Smoking status (yes/no) as of the beginning of
employment and clinical signs of potential chromium irritation were 
identified from company records. Results Cumulative hexavalent
chromium exposure showed a strong dose-response relationship for lung 
cancel: Clinical signs of irritation, cumulative trivalent
chromium exposure, and duration of work were not found to be associated 
with a risk of lung cancer when included in a proportional
hazards model with cumulative hexavalent chromium exposure and smoking. 
Age-specific data on cumulative hexavalent chromium
exposure, observed and expected numbers of lung cancer cases, and 
person-years of observation are provided Conclusion Cumulative
hexavalent chromium exposure was associated with an increased lung 
cancer risk; cumulative trivalent chromium exposure was not.
The excess risk of lung cancer associated with cumulative hexavalent 
chromium exposure was not confounded by smoking status. The
current study offers the best quantitative evidence to date of the 
relationship between hexavalent chromium exposure and lung cancel:



Rowbotham AL; Levy LS; Shuker LK 
  
Chromium in the environment: an evaluation of exposure of the UK general 
population and possible adverse health effects 
  
JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART B-CRITICAL REVIEWS 
2000,   3,    3, pp 145-178 
  
Chromium in the hexavalent form, Cr(VI), has long been recognized as a 
carcinogen and there is concern as to the effects of
continuous low-level exposure to chromium both occupationally and 
environmentally. This review summarizes the available exposure
data and known health effects and evaluates the potential risk to human 
health in the United Kingdom. Chromium emissions to the
environment in the United Kingdom are predominantly derived from fuel 
combustion, waste incineration, and industrial processes. The
less toxic trivalent form of chromium [Cr(III)] is dominant in most 
environmental compartments, and any Cr(VI), the more toxic form,
that is emitted to the environment can be reduced to Cr(III). Food is a 
major source of exposure to chromium, and estimated daily oral
intakes Tor infants (1 yr), children (11 yr), and adults are 33-45, 
123-171, and 246-343 mu g/person/d, respectively Soil ingestion,
particularly common in young children, can contribute to oral intake. 
Inhalation is a minor route of exposure for the general population.
Average daily inhalation intakes in infants can range from 0.004 mu g/d 
for rural infants to 0.14 mu g/d for urban infants who are
passively exposed to tobacco smoke, whereas adults who live in 
industrialized areas and smoke may take up between 2 and 12 mu
g/d. The most serious health effect associated with Cr(VI) is lung 
cancer, which has been associated with some occupational exposure
scenarios, whereas Cr(III) is an essential nutrient with a broad safety 
range and low toxicity. The human body has effective
detoxification mechanisms that can reduce ingested or inhaled Cr(VI) to 
Cr(III). In con clusion, there is no clear evidence to relate
exposure to environmental levels of chromium with adverse health effects 
in either the general UK population or subgroups exposed to
chromium around industrialized or contaminated sites. It can be expected 
that an improved understanding of the relevance of possible
long-term accumulation of Cr(III) in the body may facilitate a more 
complete assessment, in the future, of the health risks in the general
population associated with environmental exposure to chromium. 
 Source item page count: 


 
De Flora S 
  
Threshold mechanisms and site specificity in chromium(VI) carcinogenesis 
  
CARCINOGENESIS 2000,   21,    4, pp 533-541 
  
Ten gears have elapsed since the International Agency for Research on 
Cancer (IARC) evaluated the carcinogenicity of chromium and
chromium compounds. Further studies performed during the last decade 
have provided further epidemiological, experimental and
mechanistic data which support the IARC conclusions. A wealth of results 
indicate that, at variance with chromium(0) and
chromium(III), chromium(VI) can induce a variety of genetic and related 
effects in vitro. The lack of carcinogenicity of chromium(0)
and chromium(III) compounds in experimental animals is well established, 
and only a minority of animal carcinogenicity data with
chromium(VI) compounds were positive (30 out of 70, i.e. 42.9%). 
Moreover, most positive studies used administration routes which
do not mimic any human exposure and by-pass physiological defense 
mechanisms. Typically, positive results were only obtained at
implantation sites and at the highest dose tested. Exposure to 
chromium(VI) has been known for more than a century to be associated
with induction of cancer in humans. Carcinogenicity requires massive 
exposures, as is only encountered in well defined occupational
settings, and is site specific, being specifically targeted to the lung 
and, in some cases, to the sinonasal cavity. Increased death rates for
cancers at other sites, which were occasionally reported in some 
epidemiological studies, were almost invariably not statistically
significant, and inconsistent (being counterbalanced by other studies 
which apparently showed decreased rates for the same cancers).
As we recently quantified in human body compartments, chromium(VI) can 
be reduced in body fluids and non-target cells, which
results in its detoxification, due to the poor ability of chromium(III) 
to cross cell membranes. In target cells, chromium(VI) tends to be
metabolized by a network of mechanisms leading to generation of reduced 
chromium species and reactive oxygen species, which will
result either in activation or in detoxification depending on the site 
of the intracellular reduction and its proximity to DNA. When
introduced by the oral route, chromium(VI) is efficiently detoxified 
upon reduction by saliva and gastric juice, and sequestration by
intestinal bacteria. If some chromium(VI) is absorbed by the intestine, 
it is massively reduced in the blood of the portal system and then
in the liver. These mechanisms explain the lack of genotoxicity, 
carcinogenicity, and induction of other long-term health effects of
chromium (VI) by the oral route. Within the respiratory tract, 
chromium(VI) is reduced in the epithelial-lining fluid, pulmonary 
alveolar
macrophages, bronchial tree and peripheral lung parenchyma cells. Hence, 
lung cancer can only be induced when chromium(VI) doses
overwhelm these defense mechanisms. The efficient uptake and reduction 
of chromium(VI) in red blood cells explains its lack of
carcinogenicity at a distance from the portal of entry into the body. 
All experimental and epidemiological data, and the underlying
mechanisms, point to the occurrence of thresholds in chromium(VI) 
carcinogenesis. 




Barceloux DG 
  
Chromium 
  
JOURNAL OF TOXICOLOGY-CLINICAL TOXICOLOGY 1999,   37,    2, pp 173-194 
  
Chromium occurs primarily in the trivalent state (III), which is the 
most stable form, or in the hexavalent state (VI), which is a strong
oxidizing agent. Elemental chromium (0) does not occur naturally on 
earth. Trivalent chromium (III) is an essential trace metal necessary
for the formation of glucose tolerance factor and for the metabolism of 
insulin. Commercial applications of chromium compounds
include tanning (III), corrosion inhibition, plating, glassware-cleaning 
solutions, wood preservatives (VI), manufacture of safety
matches, metal finishing (VI), and the production of pigments (III, VI). 
Hexavalent chromium (VI) contaminated local soil when
chromium waste slag was part of the fill material present in 
residential, public, and industrial areas. In some urban areas, about
two-thirds of the chromium in air results from the emission of 
hexavalent chromium from fossil fuel combustion and steel production.
The remaining chromium in air is the trivalent form. The residence time 
of chromium in air is <10 days, depending on the particle size.
Trivalent compounds generally have low toxicity and the gastrointestinal 
tract poorly absorbs these compounds. Hexavalent chromium
is a skin and mucous membrane irritant and some of these hexavalent 
compounds are strong corrosive agents. Hexavalent chromium
compounds also produce an allergic contact dermatitis characterized by 
eczema. Sensitivity to trivalent compounds is much less
frequent, but some workers may react to high concentrations of these 
compounds. Hexavalent chromium is recognized by the
International Agency for Research on Cancer and by the US Toxicology 
Program as a pulmonary carcinogen. The increased risk of
lung cancer occurs primarily in workers exposed to hexavalent chromium 
dust during the refining of chromite ore and the production of
chromate pigments. Although individual studies suggest the possibility 
of an excess incidence of cancer at sites outside the lung, the
results from these studies are inconsistent. 
 


Droste JHJ; Weyler JJ; Van Meerbeeck JP; Vermeire PA; van Sprundel MP 
  
Occupational risk factors of lung cancer: a hospital based case-control 
study 
  
OCCUPATIONAL AND ENVIRONMENTAL MEDICINE 1999,   56,    5, pp 322-327 
  
Objectives-To investigate the relation between lung cancer and exposure 
to occupational carcinogens in a highly industrialised region in
western Europe. Methods-in a case-control study 478 cases and 536 
controls, recruited from 10 hospitals in the Antwerp region,
were interviewed. Cases were male patients with histologically confirmed 
lung cancer; controls were male patients without cancer or
primary lung diseases. Data were collected by questionnaires to obtain 
information on occupations, exposures, and smoking history.
Job titles were coded with the Office of Populations, Censuses and 
Surveys industrial classification. Exposure was assessed by self
report and by job-task exposure matrix. Exposure odds ratios were 
calculated with logistic regression analysis adjusted for age,
smoking history, and marital and socioeconomic status. Results-A job 
history in the categories manufacturing of transport equipment
other than automobiles (for example, shipyard workers), transport 
support services (for example, dockers), and manufacturing of metal
goods (for example, welders) was significantly associated with lung 
cancer (odds ratios (ORs) 2.3, 1.6, and 1.6 respectively). These
associations were independent of smoking, education, civil, and economic 
status. Self reported exposure to potential carcinogens did
not show significant associations with lung cancer, probably due to 
nondifferential misclassification. Then assessed by job-task
exposure matrix, exposure to molybdenum, mineral oils, and chromium were 
significantly associated with lung cancer. A strong
association existed between smoking and lung cancer: OR of ex-smokers 
4.2, OR of current smokers 14.5 upsilon non-smokers.
However, smoking did not confound the relation between occupational 
exposure and lung cancer. Conclusions-The study has shown a
significant excess risk of lung cancer among workers in manufacturing of 
metal goods, manufacturing of transport equipment (other than
automobiles), and transport support services. Assessment of exposure to 
specific carcinogens resulted in significant associations of
chromium, mineral oils, and molybdenum with lung cancer. This study is, 
to our knowledge, the first study reporting a significant
association between occupational exposure to molybdenum and lung cancer. 
 


 
Kimbrough DE; Cohen Y; Winer AM; Creelman L; Mabuni C 
  
A critical assessment of chromium in the environment 
  
CRITICAL REVIEWS IN ENVIRONMENTAL SCIENCE AND TECHNOLOGY 1999,   29,    
1, pp 1-46 
  
This article reviews the emissions, environmental fate and transport, 
analytical chemistry, uptake and metabolism, toxicology, and
human epidemiology of chromium. Chromium is unique among regulated toxic 
elements in the environment in that different species of
chromium, specifically chromium (III) and chromium (VI), are regulated 
in different ways. in contrast to other toxic elements where the
oxidation state is not distinguished. In both industrial and 
environmental situations chromium (III) and chromium (VI) can 
inter-convert,
with reduction of chromium (VI) to chromium (III) generally being 
favored in most environmental situations. Chromium released into
the air, water, and soil can be transported among the various 
environmental media through various intermedia transport processes.
Once in the environment, chromium can be taken up by human and other 
ecological receptors. Chromium (III) is generally absorbed
through cell membranes albeit to a significantly lesser degree than 
chromium (VI). Because most of the biosphere is reducing for
chromium (VI) and chromium (III) is relatively immobile, there is little 
bioconcentration or biomagnification of chromium (VI).
Chromium appears to be a nutrient for at least some plants and animals, 
including humans, although chromium (VI) species have been
reported to be toxic to bacteria, plants, and animals. Human toxicity 
includes lung cancer, liver, kidney and gastric damage, and
epidermal irritation and sensitization. However, it is noted that 
medical, toxicological, and epidemiological evidence suggests that not 
all
compounds containing chromium (VI) species (e.g., chromate salts) are 
carcinogenic.