Journal of Environmental Protection, 2011, 2, 533-536
doi:10.4236/jep.2011.25061 Published Online July 2011 (http://www.scirp.org/journal/jep)
Occupational Exposure to Paints Causes
Impairment of Kidney Functions
Saeed S. Al-Ghamdi
Department of Pharmacology and Toxicology, Faculty of Medicine, Umm Al-Qura University, Makkah, Kingdom of Saudi Arabia.
Received April 13th, 2011; revised May 21st, 2011; accepted June 27th, 2011.
ABSTRACT
It has been suggested that exp osure to organic solvents may have a role in the impa irment of kidney function that may
progress to kidney failure. However, this has never been evaluated with an appropriate analytical study of the kidney
functions of those people who are chronically exposed to these chemicals. This study was designed to measure the kid-
ney function of car painters in the city of Makkah, Saudi Arabia. Fifty workers were selected at random for this study
and compared to thirty male medical students wh o were taken as a control grou p. Blood samples were co llected for the
analysis of kidney function. The levels of blood urea nitrogen (BUN), creatinine, and uric acid were scientifica lly high-
er in the tested group compared to the control group. In addition to this, the levels of these parameters were signifi-
cantly higher in the serum of car painters who worked in this industry for more than ten years compared to painters
who worked for less than ten years. Moreover, the number of car painters who were not using protective gloves and
masks during working hours were 43 and the number of car painters who visited specialized clinics because of kidney
problems were 45 of the 50 tested volunteers. These findings support the hypothesized association of solvent exposure
with the development of chronic renal failure. They should prompt clinicians to give greater attention to patients’ oc-
cupational exposures. Routine monitoring of kidney functions and the use of protective materials are of greater impor-
tance to minimize the occupationa l diseases caused by organic solvents.
Keywords: Organic Sol vents, Uric Acid, Creatinine, BUN, Kidney
1. Introduction and Methods
An occupational disease is any chronic ailment that
occurs as a result of work or occupational activity. It is
an aspect of occupational safety and health, typically
identified when it is shown that it is more prevalent in a
given body of workers than in the general population, or
in other worker populations.
Occupational renal diseases provide models for under-
standing environmental renal diseases. Kidney damage in
few workers induced by heavy exposure to identifiable
toxins indicates what to expect among the large popula-
tion exposed to low levels of organic solvents dispersed
in the larger environment [1,2]. Organic solvents are a
class of chemical substances that are widely used in large
volume in various manufacturing products including the
paints. The possible role of organic solvent exposure in
the development and/or the progression of chronic renal
failure still is a controversial scientific issue more than
forty years after the earliest study by Beirne and Brennan
[3].
Many epidemiological and recent experimental studies
were conducted to prove the effects of these chemicals
on kidneys and define the mechanism of action [4-8].
Although some of these studies were criticized for their
methodological weaknesses with respect to sample size
and inaccuracy in case of definition or exposure assess-
ment, most of them showed significant associations of
solvent exposure with various types of kidney disorders
[9-13]. These studies, however, never tested the kidney
function of people with occupational chronic exposure to
organic solvents. I therefore investigated the effect of
organic solvent exposures in a cohort of fifty volunteer
car painters with the mean of the serum level of uric acid,
creatinine and blo od urea nit r ogen (BUN).
2. Materials and Methods
2.1. Exposure Assessment
Fifty male volunteer painters were asked about their life-
time occupational activities by train ed interviewers using
a questionnaire designed for this purpose. For each vol-

Occupational Exposure to Paints Causes Impairment of Kidney Functions 534
unteer; age, nationality, duration of exposure, health stat us,
and use of protective materials were recorded. Working
conditions and frequ ency of use (every day, at least once
a week, occasionally) were also recorded. Thirty male
volunteer medical students were used as a negative con-
trol for this study.
2.2. Kidney Function Analysis
Blood samples were collected for measuring the levels of
uric acid, BUN, and creatinine using the Dimension
Xpand plus instrument, Dade behring, USA.
2.3. Statistical Analysis
Results are presented as mean  S.E.M. Means were ob-
tained from six rats from each group. Statistical analysis
was performed using one way ANOVA (Kruskal Wallis
test) except for the diuretic activity where the Mann
Whitney test was used, and the statistical significance
was assured when P < 0.05.
3. Results
3.1. Blood Analysis
Kidney function tested for the uric acid, creatinene and
BUN all showed significantly higher (P < 0.05) levels of
these parameters in the serum of the car painters com-
pared to the control group (Figure 1).
3.2. Duration of Exposure
Analysis of the car painters’ duration of exposure shows
that the level of the uric acid, creatinine, and BUN in the
serum of the tested volunteers who worked for more than
ten years in the car painting industry were significantly
higher (P < 0.05) than those who spent less than ten
years in the industry (Figure 2).
3.3. Use of Protective Materials
According to the questionnaire records, only seven out of
fifty volunteer car painters were using protective gloves
and masks during their working hours (Figure 3).
0
2
4
6
8
10
12
14
CR EA TIN IN EU RIC ACIDBU N
mg/dL
TE ST
CONTROL
Figure 1. Serum levels of the uric acid, creatinine, and BUN
of the studied groups.
0
2
4
6
8
10
12
14
CREATININEURIC ACIDBUN
mg/dL
>1 0 ye aar s
<1 0 ye aar s
Figure 2. Comparing the levels of serum uric acid, create-
nine and BUN in car painters who were exposed for more
than ten years with those who were exposed for less than
ten years.
Figure 3. Numbers of painters who were using gloves and
masks during work hours.
3.4. Complaining of Kidney Disorders
According to the questionnaire records, car painters who
visited hospital complaining of kidney pain were higher:
43 out of 50 (Fig ur e 4).
4. Discussion
Due to their high lipophilicity, organic solvents may cause
physiochemical damage to the renal glomeruli and tubule
[14]. Moreover, short-term exposure to these solvents have
been shown to cause tubular necrosis, a life-threatening
situation characterized by oliguria and azotemia [15,16].
By observational assessment of the work place, I noticed
that all areas I visited were semi-closed with n o adequate
ventilation, which meant that painters’ exposure to sol-
vents exceeded the threshold limit value recommended
for the mixture by the American Conference of Govern-
mental Industrial Hygienists (ACGIH).
Several recent studies have suggested that a relation-
may exist between exposure to occupational organic sol-
vents (gasoline, gasoline-based paint spray, jet fuel, min-
eral turpentine) and diseases of the kidney, particularly
malignancy and various forms of glomerulonephritis [17-
C opyright © 2011 SciRes. JEP

Occupational Exposure to Paints Causes Impairment of Kidney Functions535
0
10
20
30
40
50
Complain
No complain
Figure 4. Number of car painters in the tested group who
complained of kidney pain.
21]. Retrospective exposure assessment was a critical
issue in many of the previous studies. My method is
based on a detailed and structured questionnaire and
blind evaluation of exposures by experienced car painters
and has proven to be very reliable. An important strength
of this study, is that I assessed the kidney function of
people who were chronically exposed to paints that con-
tain organic solvents and noticed the higher levels of
serum creatinine, uric acid and BUN of the painter over
the control. My findings are strongly supported by re-
cording the painters who visited urologists for kidney
problems. These findings are independent of age and eth-
nicity.
Different mechanisms of action are probably response-
ble for the initial events leading to renal tubular cell
damage. Unfortunately, for the majority of solvents, the
early critical effects are still speculative. The h igh serum
levels of creatinine, uric acid and BUN are considered to
be indicators for the damaging of the tubular epithelium.
Fortunately, nephrotoxicity caused by organic solvents is
reversible once the exposure has ceased. The damaging
of tubular epithelium can be recovered, where it takes
about three weeks for the tubular epithelium to regene-
rate. Recovery may be complete, but depending on the
severity of the intoxication and the previous status of
renal function, some degree of renal insufficiency may
persist [13].
The solvent exposure was associated with increased-
baseline proteinuria and the relationship with end-stage
renal disease (ESRD) [18]. This relationship tends to
weaken after adjustment and suggests that solvent ne-
phrotoxicity may be mediated partly by enhancing pro-
teinuria, a major risk factor for kidney disease progres-
sion. In support of this hypothesis, several occupational
studies have shown that workers who were exposed to
various types of solvents (both aliphatic and aromatic
hydrocarbons) had higher levels of albuminuria as well
as low molecular weight proteinuria, which is consid-
ered to be a marker of tubular injury, as compared with
non-exposed work ers [19-21].
The limitation of this study, which should be noted, is
urine analyses for protein because of technical reasons.
However, previous cohort and cross-sectional studies
[22-24], which have proven the association between
chronic exposure to solvents and albuminurea seem to be
adequate. Occupational renal diseases are important be-
cause they are entirely preventable. For this reason, the
majority of car painters in this study who were not using
the protective materials during painting complained of
kidney problems and visited specialist clinics for consul-
tation. In addition, renal disease produced by heavy ex-
posure to industrial toxins by relatively few workers pro-
vides a clinical basis for understanding the consequences
of low-dose exposure to the general population from en-
vironmental pollutants. The known toxins that produce
kidney disease in the workplace are limited to the heavy
metals plus silica and certain organic compounds, par-
ticularly halogenated hydrocarbons, employed as Indus-
trial solvents [16]. However, the absence of information
on the adverse renal effects of other industrial pollutants
does not prove that no such effects occur. In this study,
the relationship between the background of the painters
and the impairment of the kidney function were not sig-
nificant. Even though, the probability that the genetic
basis of individual susceptibility can not be neglected.
The contribution of organic solvents to renal disease of
painters based on individual susceptibility may become
clearer after certain genetic polymorphism investigations.
5. Conclusions
It can be concluded that these results corrobo rate with an
association between renal disorders and exposure to or-
ganic solvents. They provide new evidences of the po-
tential role of so lvents in the development of k idney dis-
eases. This might be prevented by using protective mate-
rials and carrying out routine tests of kidney function.
6. Acknowledgments
This study was supported by a grant from the Center for
Medical and Medical Sciences Researches, Umm Al-Qura
University.
REFERENCES
[1] T. Ehrenreich, “Renal Disease from Exposure to Sol-
vents,” Annals of Clinical and Laboratory Science, Vol. 7,
No. 1, 1977, pp. 6-16.
[2] Wedeen, “Occupational and Environmental Renal Dis-
ease,” Seminars in Nephrology, Vol. 17, No. 1, 1997, pp.
46-53.
[3] G. J. Beirne and J. T. Brennan, “Glomerulonephritis As-
sociated with Hydrocarbon Solvents: Mediated by An-
tiglomerular Basement Membrane Antibody,” Arch En-

Occupational Exposure to Paints Causes Impairment of Kidney Functions 536
viron Health, Vol. 25, 1972, pp. 365-369.
[4] E. T. O’Brien, W. O. Yeomn and J. A. E. Hobby, “Hepa-
torenal Damage from Toluene in ‘Glue Sniffer’,” British
Medical Journal, Vol. 2, 1971, pp. 29-30.
[5] S. M. Taher, R. J. Anderson, R. McCartney, M. M.
Poputzer and R. W. Schirer, “Renal Tubular Acidosis
Associated with Toluene ‘Sniffing’,” The New England
Journal of Medicine, Vol. 290, No. 14, 1974, pp. 765-768.
doi:10.1056/NEJM197404042901403
[6] A. H. Moss, P. A. Gabow and W. D. Kahney, “Fanconi’s
Syndrome and Distal Renal Tubular Acidosis after Glue
Sniffing,” Annals of Internal Medicine, Vol. 92, 1980, pp.
69-70.
[7] H. Z. Screicher, P. A. Gabow, A. H. Moss, D. Kono and
W. D. Kaehny, “Syndrome of Toluene Sniffing in
Adults,” Annals of Internal Medicine, Vol. 94, 1981, pp.
758-762.
[8] G. Venkatamran, “Renal Damage and Glue Sniffing,”
British Medical Journal, Vol. 283, No. 6304, 1981, p.
1467. doi:10.1136/bmj.283.6304.1467-a
[9] W. E. Daniell, W. G. Couser and L. Rosenstock, “Occu-
pational Solvent Exposure and Glomerulonephritis: A
Case Report and Review of the Literature,” Journal of the
American Medical Association, Vol. 259, 1988, pp.
2280-2283. doi:10.1001/jama.259.15.2280
[10] C. M. Fored, G. Nise, E. Ejerblad, J. P. Fryzek, P. Lind-
blad, J. K. McLaughlin, C. G. Elinder and O. Nyren,
“Absence of Association between Organic Solvent Ex-
posure and Risk of Chronic Renal Failure: A Nationwide
Population-Based Case-Control Study,” Journal of the
American Society of Nephrology, Vol. 15, No. 1, 2004, pp.
180-186. doi:10.1097/01.ASN.0000103872.60993.06
[11] U. Ravnskov, “Hydrocarbons May Worsen Renal Func-
tion Inglomerulonephritis: A Meta-Analysis of the Case-
Control Studies,” American Journal of Industrial Medi-
cine, Vol. 37, No. 6, 2000, pp. 599-606.
doi:10.1002/(SICI)1097-0274(200006)37:6<599::AID-AJ
IM4>3.3.CO;2-O
[12] S. S. Al-Ghamdi, D. A. Allen, M. J. Raftery and M. M.
Yaqoob, “Organic Solvent-Induced Proximal Tubular
Cell Toxicity via Caspase-3 Activation,” Clinical Toxi-
cology, Vol. 41, No. 7, 2003, pp. 941-945.
doi:10.1081/CLT-120026515
[13] S. S. Al-Ghamdi, M. J. Raftery and M. M. Yaqoob,
“Acute Solvent Exposure Induced Activation of Cyto-
chrome P4502E1 Causes Proximal Tubular Cell Necrosis
by Oxidative Stress,” Toxicology in Vitro, Vol. 17, 2003,
pp. 335-3412. doi:10.1016/S0887-2333(03)00021-3
[14] A.Sato, I. Yonekura, T. Kaneko and T. Koizumi, “Renal
Disorders Induced by Organic Solvents,” Sangyo Igaku,
Vol. 30, No. 2, 1988, pp. 85-96.
[15] H. Savolainen, H. Vainio, M. Helojoki and E. Elovaara,
“Biochemical and Toxicological Effects of Short-Term,
Intermittent Xylene Inhalation Exposure and Combined
Ethanol Intake,” Archives of Toxicology, Vol. 41, No. 3,
1978, pp. 195-205. doi:10.1007/BF00354091
[16] R. Lauwerys, A. Bernard, C. Viau and J. P. Buchet,
“Kidney Disorders and Hematotoxicity from Organic
Solvent Exposure,” Scandinavian Journal of Work, Envi-
ronment & Health, Vol. 11, No. 2, 1985, pp. 83-90.
[17] J. M. Harrington, H. Whitby , C. N. Gray, F. J. Reid, T. C.
Aw and J. A. Waterhouse, “Renal Disease and Occupa-
tional Exposure to Organic Solvents: A Case Referent
Approach,” British Journal of Industrial Medicine, Vol.
46, No. 9, 1989, pp. 643-50.
[18] S. Jacob, M. He´ry, J. C. Protois, J. Rossert and B.
Stengel, “Effect of Organic Solvent Exposure on Chronic
Kidney Disease Progression: The GN-progress Cohort
Study,” Journal of the American Society of Nephrology,
Vol. 18, No. 1, 2007, pp. 274-281.
doi:10.1681/ASN.2006060652
[19] A. Mutti, T. Coccini, R. Alinovi, G. Toubeau, F.
Broeckaert, E. Bergamaschi, P. Mozzoni, D. Nonclercq,
A. Bernard and L. Manzo, “Exposure to Hydrocarbons
and Renal Disease: An Experimental Animal Model,”
Ren Fail, Vol. 21, 1999, pp. 369-385.
doi:10.3109/08860229909085101
[20] Van Der Laan, “Chronic Glomerulonephritis and Organic
Solvents. A Case-Control Study,” International Archives
of Occupational and Environmental Health, Vol. 47, No.
1, 1980, pp. 1-8.
[21] P. Hotz, “Occupational Hydrocarbon Exposure and
Chronic Nephropathy,” Toxicology, Vol. 90, No. 3, 1994,
pp. 163-283. doi:10.1016/0300-483X(94)90091-4
[22] D. M. Hashimoto, K. T. Kelsey, T. Seitz, H. A. Feldman,
B. Yakes and D. C. Christiani, “The Presence of Urinary
Cellular Sediment and Albuminuria in Newspaper Press-
workers Exposed to Solvents,” Journal of Occupational
and Environmental Medicine, Vol. 33, No. 4, 1991, pp.
516-26.
[23] G. Remuzzi and T. Bertani, “Pathophysiology of Progres-
sive Nephropathies,” The New England Journal of Medi-
cine, Vol. 339, 1998, pp. 1448-1456.
doi:10.1056/NEJM199811123392007
[24] D. Solet and T. G. Robins, “Renal Function in Dry
Cleaning Workers Exposed to Perchloroethylene,”
American Journal of Industrial Medicine, Vol. 20, No. 5,
1991, pp. 601-14. doi:10.1002/ajim.4700200504