J Gandhara Med Dent Sci

October - December 2025

ORIGINAL ARTICLE

ESSENTIAL AND TOXIC TRACE METALS STATUS IN CHRONIC HASHISH CONSUMERS:

EVIDENCE FROM A PAKISTANI COHORT

Asmat Ullah

, Abad Khan

, Asif Ali

How to cite this article

Ullah A, Khan A, Ali A. Essential and

Toxic Trace Metals Status in Chronic

Hashish Consumers: Evidence from A

Pakistani Cohort. J Gandhara Med Dent

Sci.2025;12(3):3-8.https://doi.org/10.37

762/jgmds.12-4.755

Date of Submission: 09-07-2025

Date Revised: 09-09-2025

Date Acceptance: 10-09-2025

Associate Professor & Chairman,

Department of Pharmacy, The

University of Swabi

M.Phil Scholar, Department of

Pharmacy, The University of Swabi

Correspondence

Asmat Ullah, PhD Scholar,

Department of Pharmacy, The

University of Swabi

+92-321-9014220

asmat.pharmd@gmail.com

ABSTRACT

OBJECTIVES

Chronic hashish consumption may inﬂuence trace metal homeostasis and

promote oxidative stress. This study aimed to evaluate serum concentrations

of essential and toxic trace elements-iron (Fe), copper (Cu), zinc (Zn), lead

(Pb), and cadmium (Cd) - in long-term hashish users.

METHODOLOGY

A cross-sectional study was conducted in Peshawar, Pakistan, involving 104

adult males aged 25–60 years, divided into chronic hashish users (n = 53)

and non-users (n = 51). Venous blood samples were collected and analyzed

for trace metal content using ﬂame atomic absorption spectrophotometry

(FAAS) following nitric and perchloric acid digestion.

RESULTS

Mean serum concentrations of Fe (2.6 ± 0.3 µg/dL) and Cu (0.5 ± 0.1 µg/dL)

were signiﬁcantly elevated in hashish users compared to non -users (2.4 ± 0.2

µg/dL and 0.3 ± 0.02 µg/dL, respectively; p ≤ 0.05). No signiﬁcant

diﬀerences were observed in Zn, Pb, or Cd levels. Pearson's correlation

revealed no signiﬁcant association between trace metal levels and either

duration or quantity of hashish use.

CONCLUSION

Elevated iron and copper levels in hashish users suggest a potential

disturbance in the regulation of redox-active metals. While this may

contribute to oxidative stress, direct biomarkers were not assessed in the

current study. Further mechanistic studies are warranted to conﬁrm this link.

KEYWORDS: Hashish, Trace Elements, Metalloenzymes, Cell Injury, Free

Radicals, Oxidative Stress

INTRODUCTION

Metals are indispensable for maintaining physiological

homeostasis, playing critical roles in enzymatic activity,

signal transduction, and protein stabilization. They

serve as essential cofactors for metalloenzymes, which

catalyze numerous metabolic reactions.

1,2

Trace

amounts of essential elements, such as iron, calcium,

magnesium, copper, manganese, and zinc, are vital for

growth, immune function, and neurological

development.

3,4

The regulatory balance of these metal

ions is tightly controlled; however, dysregulation-

whether due to environmental exposure or

physiological disorders-can result in excessive metal

accumulation, aberrant binding to non-target proteins,

and ensuing cellular damage.

Such disruptions impair

protein conformation and mitochondrial integrity,

ultimately provoking apoptosis or necrosis.

Human

exposure to abnormal metal levels originates from

multiple sources, including industrial processes (such as

mining, metalworking, and leather tanning),

contaminated groundwater, agricultural runoﬀ, and

environmental pollution.

Numerous studies have

conﬁrmed heavy metal toxicity in these settings, linking

it to neurodegenerative, renal, and reproductive

disorders.

8,9

A central mechanism of metal-induced

toxicity is oxidative stress. Overabundant essential

metals (e.g., Fe, Cu, Mn) can trigger Fenton and Haber–

Weiss reactions, generating ROS such as hydroxyl

radicals, hydrogen peroxide, and singlet oxygen.

10,11

Meanwhile, non-essential metals such as lead,

cadmium, and mercury disrupt mitochondrial electron

transport and deplete antioxidants, including

glutathione, thereby further increasing ROS levels.

12,13

This oxidative imbalance damages cellular lipids,

proteins, and DNA, contributing to the development of

more than 50 diseases, including cancer, cardiovascular

disease, diabetes, neurodegenerative disorders, and

autoimmune conditions.

14,15,16

Speciﬁcally, ROS-

induced genomic instability and lipid peroxidation drive

chronic inﬂammation, mutagenesis, and tissue

degeneration. Metallothioneins and metallochaperones

are intracellular proteins that bind metals, regulating

their distribution and buﬀering against oxidative stress

within cells.

17,18

However, excessive metal exposure

can overwhelm these protective systems, leading to

metal dysregulation and sustained oxidative stress.

Cannabis plants-especially in unregulated harvests-

frequently accumulate heavy metals from soil and

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October - December 2025

cultivation processes, potentially exposing consumers

to lead, cadmium, chromium, nickel, and mercury. For

example, seedlings grown in metal-rich soils have

shown concentrations of cadmium and lead exceeding

WHO limits.

19,20

A meta-analysis has conﬁrmed that

cannabis

‘

s high bioaccumulation potential poses risks

through consumption, particularly in smoking forms,

which allow high pulmonary absorption.

Epidemiological data from NHANES (>7,000 adults)

indicate that exclusive marijuana users have 22–27%

higher blood lead and cadmium levels compared to

non-users, even after adjusting for confounding

factors.

21,22

Emerging evidence also suggests that

cannabis itself may disrupt oxidative balance.

Experimental and clinical studies report reduced

activity of antioxidant enzymes such as superoxide

dismutase (SOD) and glutathione peroxidase in

cannabis users, accompanied by elevated lipid

peroxidation and DNA oxidation.

Such disturbances

may contribute to cardiometabolic dysfunction, altered

lipid proﬁles, and renal impairment, which could act

synergistically with metal-induced oxidative stress.

Thus, cannabis use may impose a dual toxicological

burden: direct redox disruption and enhanced heavy

metal exposure.

24,25

In South Asia, cannabis use is

particularly relevant. According to the UNODC’s 2020

Pakistan Drug Use Survey, an estimated four million

individuals consume cannabis, with the highest

prevalence in Khyber Pakhtunkhwa province.

Populations in that region may therefore face elevated

oxidative stress and trace metal imbalance due to

chronic hashish use.

Past studies have also

demonstrated that substance abuse-including tobacco,

alcohol, opioids, and cannabis-is linked to altered serum

trace element proﬁles and weakened antioxidant

defenses.

21,22

However, little is known about the

speciﬁc impact of chronic hashish consumption on trace

metal homeostasis, particularly in South Asian

populations where cannabis use is widespread. Given

that iron and copper are central regulators of redox

biology and oxidative stress, and that cannabis plants

readily bioaccumulate toxic metals from their growing

environment, investigating these elements in habitual

users is of considerable biochemical and public health

relevance. The present study, therefore, quantiﬁes

serum concentrations of iron, copper, zinc, lead, and

cadmium in chronic hashish users from Khyber

Pakhtunkhwa, Pakistan, providing novel evidence on

potential metal-related disturbances associated with

long-term cannabis exposure.

METHODOLOGY

This cross-sectional study was conducted over 12

months in 2018-2019 in rural communities located near

the University of Peshawar. The source population

comprised adult males aged 25-60 years residing in

these communities. Data on socio-demographic

characteristics and baseline clinical parameters were

obtained using a structured questionnaire, which

included variables such as age, body weight, blood

pressure, duration of hashish consumption, and the

average quantity of hashish used per day, calculated

based on self-reported lifetime usage. The questionnaire

was developed after reviewing relevant literature,

reviewed by two pharmacologists and a public health

researcher for content validity, and pilot-tested in 10

individuals to assess clarity and feasibility before being

applied in the entire study. The required sample size

was estimated using an independent samples t-test,

assuming a medium eﬀect size (Cohen’s d = 0.5), α =

0.05, and power (1–β) = 0.80, which yielded a

minimum of 51 participants per group. To account for

potential dropouts, slightly larger numbers were

recruited, resulting in 53 chronic hashish users and 51

non-users (total n = 104). A non-probability

convenience sampling technique was employed with

the assistance of local community focal persons, as the

sensitive nature of substance use limited the feasibility

of probability-based sampling. The study was approved

by the Advanced Study and Research Board, University

of Swabi, vide Notiﬁcation No. 1(3)-Dy.Reg-

3/UOS/2017/170, dated: 14-09-2017. Ethical approval

was provided by the Ethics Committee of the

Department of Pharmacy, University of Swabi, vide

letter No. UOS/Pharm-Ethl20 181/223. All study

participants signed the informed consent form to

participate in the study. Written informed consent was

obtained from all participants prior to enrollment. Each

participant provided written informed consent after

being informed of the study’s objectives, procedures,

and conﬁdentiality measures. A total of 113 adult male

participants were recruited and categorized into two

groups: (a) chronic hashish users and (b) non-users-the

control group. Nine individuals declined to participate

due to concerns about the conﬁdentiality of their

personal information. Hashish users were identiﬁed

through direct interviews conducted with the assistance

of local focal persons nominated from each village.

These individuals were selected to facilitate participant

identiﬁcation while ensuring privacy and maintaining

the conﬁdentiality of participants’ substance use

history. Inclusion criteria for the hashish user group

were: males aged 25-60 years, with a self-reported

history of continuous hashish consumption for at least

the past ﬁve years, and no current or prior diagnosis of

major chronic illnesses such as hypertension, diabetes

mellitus, or asthma. The control group consisted of

individuals from the same geographic area and within

the same age range (25–60 years), with no history of

chronic diseases or substance use (including tobacco,

alcohol, or illicit drugs). For both the hashish user and

control groups, participants were screened for

Essential and Toxic Trace Metals Status in Chronic Hashish

J Gandhara Med Dent Sci

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smoking were also excluded to reduce the risk of

concurrent use of tobacco, alcohol, or other

psychoactive substances. Individuals who reported

regular use of these substances were excluded from the

study to minimize the confounding eﬀects on trace

metal levels. Speciﬁcally, participants with a history of

regular tobacco use were not enrolled, and among the

hashish users, those reporting habitual cigarette

tobacco-related heavy metal exposure. Analytical-grade

reagents were used throughout the study. Nitric acid

(65% purity) was obtained from Riedel-de Haën—

Sigma-Aldrich, USA, while perchloric acid (70%

purity) was procured from Scharlau Chemie, S.A.,

Spain. A certiﬁed 2% standard solution of heavy metals

in nitric acid was sourced from PerkinElmer, Inc., USA.

High-purity deionized water was prepared using a water

still (Model P-21701, Favorit, Malaysia). Working

standards were freshly prepared prior to each analysis

by diluting the stock solution to the desired

concentration. A 10% stock solution was prepared by

adding 10 mL of the certiﬁed standard to deionized

water, resulting in a ﬁnal volume of 100 mL. All

glassware and equipment used in the analysis were

thoroughly cleaned by soaking in 2% nitric acid,

followed by multiple rinses with deionized water to

eliminate contamination. To ensure analytical precision

and accuracy, all samples were analyzed in triplicate.

The instrument was calibrated regularly using certiﬁed

reference standards. Metal analysis was performed at

the Centralized Resource Laboratory (CRL) at the

University of Peshawar, Pakistan. Approximately 3 mL

of venous blood was collected aseptically from the

antecubital vein of each participant using sterile

disposable syringes. The samples were transferred into

gel clot activator tubes and centrifuged at 3500 (~2000

× g) revolutions per minute (rpm) for 10 minutes at 4°C

to obtain serum. The serum was carefully separated and

transferred to pre-cleaned, acid-washed polypropylene

tubes for further analysis. For the digestion of serum

samples prior to heavy metal analysis, 1 mL of serum

was mixed with 5 mL of concentrated nitric acid

(HNO₃) in a digestion tube and heated in a water bath at

60°C for 2 hours. Subsequently, 5 mL of perchloric

acid (HClO₄) was added to each sample, followed by an

additional 30-minute heating period at the same

temperature to complete the digestion process. The ﬁnal

volume was brought up to approximately 10 mL with

deionized water. All reagents used were of analytical

grade, and high-purity water was employed throughout

the procedure to minimize contamination risk.

Centrifugation was performed using a Centurion

Centrifuge (Centurion Scientiﬁc Ltd., UK).

Quantiﬁcation of serum trace metal concentrations was

carried out using a ﬂame atomic absorption

spectrophotometer (AAS), Model AAnalyst 700

(PerkinElmer Inc., USA), equipped with an automatic

Table 1: Atomic Absorption Spectrophotometric Speciﬁcations

MET

Parameter

Air

(L/min)

Acetyle

ne(L/mi

in)

Lamp

Curre

nt (A)

Slit

Width

(nm)

Wavelen

gth (nm)

Detecti

on Limits

(mg/L)

Iron 17 02 30 0.2 248.3 0.0150

Zinc 17 02 15 0.7 213.9 0.0015

Copper 17 02 15 0.7 324.8 0.0015

Lead 17 02 10 0.7 283.3 0.0150

Cadmiu

17 02 04 0.7 288.8 0.0008

background correction system and metal-speciﬁc

hollow-cathode lamps (HCLs). Instrumental

parameters, including wavelength, lamp current, slit

width, and detection limits for each metal, are presented

in Table 1.

Statistical analyses were conducted using GraphPad

Prism (version 5.01; GraphPad Software Inc., San

Diego, CA, USA). Descriptive statistics were calculated

and presented as mean ± standard deviation (SD).

Group comparisons between hashish users and non-

users were performed using an unpaired, two-tailed

Student's t-test. Normality of data distribution was

assessed using the Shapiro–Wilk test, and homogeneity

of variances was evaluated with Levene’s test. When

assumptions of normality or equal variance were not

satisﬁed, the non-parametric Mann-Whitney U test was

applied. To evaluate the relationship between the

quantity and duration of hashish consumption and

serum metal levels, Pearson’s correlation coeﬃcient (r)

was computed. A p-value ≤ 0.05 was considered

indicative of statistical signiﬁcance.

RESULTS

A total of 104 participants were enrolled, comprising 53

chronic hashish users and 51 non-users. The

demographic and clinical characteristics of both groups

are presented in Table 2. The groups did not diﬀer

signiﬁcantly in age, BMI, or blood pressure (all p >

0.05). However, total cholesterol and creatinine

clearance were signiﬁcantly higher in the hashish user

group compared with non-users (p < 0.05). The mean

serum concentrations of selected trace metals are

summarized in Table 3. Hashish users had signiﬁcantly

higher serum iron levels (2.6 ± 0.3 µg/dL) compared

with non-users (2.4 ± 0.2 µg/dL; p = 0.05). Serum

copper was also elevated in users (0.5 ± 0.1 µg/dL)

relative to controls (0.3 ± 0.02 µg/dL; p < 0.05). No

statistically signiﬁcant diﬀerences were observed for

zinc (p = 1.0), lead (p = 0.8), or cadmium (p = 0.34).

Pearson’s correlation coeﬃcients assessing the

association between hashish consumption patterns and

serum metal concentrations are presented in Table 4.

Neither the duration of hashish use nor the average

daily quantity consumed showed signiﬁcant

correlations with serum iron, copper, zinc, lead, or

Essential and Toxic Trace Metals Status in Chronic Hashish

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Table 4: Pearson Correlation between Serum Concentration of

Metals and (a) Duration of Hashish use in Years, (b) Quantity of

Hashish Use Per Day

Serum trace

metals (µg/dl)

Correlation with R-value P-value

Iron

Duration of Hashish use

(Years)

0.970 0.891

Quantitiy of Hashish use

per day (g)

0.120 0.423

Zinc

Duration of Hashish use

(Years)

-0.015 0.912

Quantitiy of Hashish use

per day (g)

-0.251 0.055

Copper

Duration of Hashish use

(Years)

0.173 0.169

Quantitiy of Hashish use

per day (g)

0.029 0.826

Lead

Duration of Hashish use

(Years)

0.033 0.981

Quantitiy of Hashish use

per day (g)

0.182 0.165

Cadmium

Duration of Hashish use

(Years)

0.210 0.221

Quantitiy of Hashish use

per day (g)

0.219 0.093

Table 2: Characteristics of the Study Subjects in the Current

Study

Parameter Non-users

(N=53)

Hashish

users(N=51)

P-Value

Mean ± SD

Age (Years) 36.8 ± 1.4 36.2 ± 6.3 0.63

BMI (Kg/m

) 22.3 ± 3.7 21.7 ± 4.8 0.11

FBS (mg/dl) 91.8 ± 8.8 90.5 ± 9.5 0.59

T. Cholesterol (mg%)

180.2 ± 22.1 211 ± 40.2 < 0.05*

CrCl (ml/min) 105.4 ± 19.2 152.2 ± 39.6 < 0.05*

Duration of Hashish

Use (Years)

N/A 19.1 ± 8.8 -

Quantity of drug

consumption per day

(gms)

N/A 3.2 ± 1.5 -

Table 3: Trace Metal Concentrations in Serum Samples of the

Study Groups in the Current Study

Serum trace metals

(µg/dl)

Non-users

(N=53)

Hashish users

(N=51)

P-Value

Mean ± SD

Iron (Fe) 2.4 ± 0.2 2.6 ± 0.3

0.05*

Zinc (Zn) 0.1 ± 0.01 0.1 ± 0.01 >0.99

Copper (Cu) 0.3 ± 0.02 0.5 ± 0.1

< 0.05*

Lead (Pb) 0.5 ± 0.01 0.6 ± 0.1 0.80

Cadmium (Cd) 0.3 ± 0.03 0.3 ± 0.05 0.34

*Statistically signiﬁcant at p < 0.05

cadmium levels (all p > 0.05).

applicable

*Statistically signiﬁcant at p < 0.05 | BMI: Body mass Index; FBS:

Fasting Blood Sugar; CrCl: Creatinine Clearance; N/A: Not

DISCUSSION

This study demonstrated signiﬁcantly elevated serum

concentrations of iron and copper among individuals

with chronic hashish use compared to non-users. Both

metals are redox-active and central to oxidative

biology, where excessive accumulation can catalyze the

formation of reactive oxygen species (ROS) through

Fenton and Haber-Weiss reactions, leading to oxidative

injury and cellular dysfunction. These ﬁndings are

consistent with earlier reports that substance abuse

alters trace metal homeostasis and weakens antioxidant

defenses.

24,25,26

Recent studies conﬁrm that iron

overload can accelerate oxidative stress-mediated tissue

injury, while copper imbalance contributes to

cardiometabolic and neurodegenerative pathologies

through mitochondrial dysfunction and redox

cycling.

26,27,28

In addition to trace metals, signiﬁcant

diﬀerences were observed in total cholesterol and

creatinine clearance between the two groups (Table 2).

The higher cholesterol levels among hashish users may

reﬂect disruptions in lipid metabolism, as cannabinoids

interact with CB1 receptors, altering appetite and

hepatic lipid synthesis. Large-scale analyses, including

NHANES, have shown associations between cannabis

use, altered lipid proﬁles, and increased

cardiometabolic risk.

Moreover, elevated iron and

copper may promote lipid peroxidation, further

aggravating dyslipidemia and atherosclerosis.

The

elevated creatinine clearance in users may represent

early glomerular hyperﬁltration, a compensatory

response linked to subclinical nephron stress, which can

progress to chronic kidney disease if sustained.

Cannabis exposure has also been implicated in altered

renal function, though results are inconsistent. Trace

metal dysregulation, particularly copper and cadmium,

may act synergistically to exacerbate renal oxidative

injury.

31,32

One plausible explanation for the elevated

iron and copper concentrations is contamination of

cannabis products during cultivation and processing,

since cannabis is a known hyperaccumulator of

environmental metals. Recent studies conﬁrm that

cannabis grown in contaminated soils can accumulate

lead, cadmium, and copper to levels exceeding WHO

safety limits.

12,33

However, since this study did not

analyze hashish samples directly, this explanation

remains speculative. Future work must include trace

metal analysis of locally consumed hashish to conﬁrm

whether environmental contamination contributes to the

observed elevations. Serum zinc levels did not diﬀer

signiﬁcantly between groups. We suggested this may

indicate preserved zinc-dependent antioxidant

responses. Zinc is a critical cofactor for antioxidant

enzymes such as superoxide dismutase (SOD).

However, without functional assays, such as measuring

SOD activity, this interpretation remains hypothetical.

Recent clinical studies report reduced SOD and

glutathione peroxidase activity in substance users

despite normal zinc concentrations, suggesting that

preserved zinc status may not translate to intact

antioxidant defense.

34,35

Future studies should therefore

incorporate enzymatic biomarkers to clarify the role of

Essential and Toxic Trace Metals Status in Chronic Hashish

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October - December 2025

zinc in cannabis-related oxidative stress. Overall, our

ﬁndings support the hypothesis that chronic hashish use

is associated with altered trace metal homeostasis,

which may contribute to oxidative stress, metabolic

dysregulation, and renal changes. Nevertheless, the

mechanisms linking cannabis exposure, environmental

contamination, and trace metal imbalance remain

incompletely understood. Future studies should

incorporate dietary intake assessments, direct analysis

of hashish products, and measurement of oxidative

stress biomarkers, ideally within larger longitudinal

cohorts that include both sexes, to elucidate causal

pathways and assess public health implications. Future

research should analyze the trace metal content of

hashish samples commonly consumed in Pakistan to

establish a direct link between cannabis use and heavy

metal exposure. Dietary assessments must be integrated

to control for nutritional inﬂuences, particularly on iron

and copper levels. Incorporation of validated

biomarkers of oxidative stress and antioxidant enzyme

activity would help clarify mechanistic pathways

linking cannabis exposure to redox imbalance. Larger,

longitudinal studies involving both men and women are

needed to improve generalizability and determine

causal and dose-response relationships. Multicenter

collaborations may also provide a broader

understanding of cannabis-related toxicological risks

across diverse populations.

LIMITATIONS

This study has several limitations that should be taken

into account when interpreting the ﬁndings. First, a

non-probability convenience sampling method was

employed, which may introduce selection bias and limit

the generalizability of the results. Second, information

on the duration and quantity of hashish use was

obtained through self-report, which is subject to recall

bias and may aﬀect accuracy. Third, the cross-sectional

design precludes any inference of causality; therefore,

longitudinal studies are necessary to establish temporal

relationships. Additionally, female participants were

excluded due to cultural sensitivities, which limited the

generalizability of the ﬁndings to males. Dietary intake,

which inﬂuences trace metal levels-particularly iron

and copper-was not assessed and may have contributed

to the observed diﬀerences. Finally, although

individuals with regular tobacco or alcohol use were

excluded, occasional or unreported smoking among

hashish users cannot be ruled out. Since tobacco is a

known source of cadmium, lead, and oxidative stress,

this remains a potential confounder. Despite these

limitations, the study also has notable strengths. To our

knowledge, it is the ﬁrst investigation from Pakistan to

evaluate essential and toxic trace metals in chronic

hashish users, thereby addressing a signiﬁcant

knowledge gap in a high-prevalence region. The use of

a locally matched control group, rigorous sample

handling, and validated atomic absorption

spectrophotometry methods enhanced the reliability of

the biochemical analyses, providing novel evidence

with public health relevance.

CONCLUSIONS

This study demonstrated signiﬁcantly elevated serum

concentrations of iron and copper in chronic hashish

users compared with non-users, suggesting disturbances

in redox-active metal regulation. While environmental

contamination of hashish may partly explain these

ﬁndings, this hypothesis was not directly tested. Other

unmeasured factors, including dietary intake,

environmental exposures, and genetic variability, could

also have inﬂuenced the results. The absence of dietary

data and functional oxidative stress biomarkers

represents an important limitation.

ACKNOWLEDGMENTS

The authors are grateful to the Higher Education

Commission of Pakistan for funding this project and to

the Centralized Resource Laboratory (CRL) at the

University of Peshawar for providing analytical

facilities. The authors are also thankful to the Study

participants.

CONFLICT OF INTEREST: None

FUNDING SOURCES:

The study was funded by the Higher Education

Commission of Pakistan through scholarship funds to

the principal author, PIN No. HEC Scholar PIN NO.

213-52616-2BM2-044, Phase II, Batch II, Indigenous

program.

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October - December 2025

AUTHORS CONTRIBUTION

The authors accept responsibility for all aspects of the work

and will ensure that any concerns regarding the accuracy or

integrity of any part are properly investigated and resolved.

Asmat Ullah - Concept & Design; Data Acquisition;

Data Analysis/Interpretation; Drafting Manuscript; Final

Approval

Abad Khan - Concept & Design; Data Acquisition; Data

Analysis/Interpretation; Drafting Manuscript; Critical

Revision; Supervision; Final Approval

Asif Ali - Concept & Design; Data Acquisition; Data

Analysis/Interpretation; Drafting Manuscript; Final

Approval

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Essential and Toxic Trace Metals Status in Chronic Hashish